The symptom signaling theory of ME/CFS involving neurons and their synapses

Holinger said:
f anyone can answer. Does Decodeme point towards or away from a narcolepsy style brain damage to something similar to orexins but with a maybe an opposite effect in ME/CFS patients? Meaning a sleep disorder but different to orexin? Is that type of damage off the table because nothing has been found so far?
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No, I don't think a negative there rules anything out.
 
Yann04 said:
@ME/CFS Skeptic

Would your theory support more organisation towards brain banks.

Or does it strictly posulate that its mostly a network problem that would thus be invisible in tissues.
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I think it would only need to explain why nothing has been found yet on the brain scans (mostly MRI) that have been done.

Based on @SNT Gatchaman interesting example of chronic traumatic encephalopathy and others' responses that neural damage would still be possible, I think brain banks and autopsies could be interesting.

There is a ZonMW project including The Netherlands' Brain Bank (NBB) that will look into this in ME/CFS.
https://projecten.zonmw.nl/nl/project/hersenveranderingen-mecvs-focus-op-het-stress-en-immuunsysteem

It would be great if something similar could be set up in the UK and Germany. Someone told me (half sarcastically) that the problem is that ME/CFS patients don't die of their disease so autopsies are not done in a systematic way.
 
Re. orexin. It is a neuropeptide. There are over 100 known neuropeptides in the human brain and the expectation is that more will be discovered.

Since they affect so many different things, including sensory perception, regulation of the vascular system, metabolism, sleep, they seem potentially relevant to ME/CFS. I remember leptin has come up before in ME/CFS, although this was in relation to its peripheral role.
 
Utsikt said:
But I have no idea if pwME/CFS have more muscles than other similarly inactive people that can still use the muscles.
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I wonder if anyone has checked for muscle activity in resting PWME. I'm imagining some signals causing the muscle cells to contract randomly; enough to qualify as exercise, but not enough firing together to move limbs noticeably.
 
EndME said:
why are we not seeing anything?
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Too difficult to measure important factors in living brains. Also, brains are very complex, so there are a lot of potential factors involved. Furthermore, the abnormalities could be limited to just a few brain cells, and the measurable factors could be limited in range and time frame. Imagine that the difference between mild ME and severe is just a few molecules in vesicles moving micrometers (nanometers?) between brain cells, leaving no trace even a few micrometers away. Astrocytes stick processes into synapse gaps, but do we know what actual molecular transfers are occurring and what's normal or abnormal?

The abnormalities might not exist post-mortem, and measuring them in live brains might be bad for live brains, at least with present technology.
 
ME/CFS Science Blog said:
But isn't that a peripheral neuropathy, one that wouldn't explain any of the core ME/CFS symptoms?

And why would a injury that is not severe cause much more debilitating fatigue symptoms than the severe CNS injuries that are already known?
If it is possible, it will probably have this special connection with the neural pathway that produces symptoms, so we're back to where we started.
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A peripheral neuropathy could be described as exaggerated/false/distorted signals reaching the brain.

When I spent time visiting SFN forums, it was obvious a portion of patients had PEM and could easily meet diagnostic criteria for ME/CFS. But the general sentiment was that ME/CFS was something to take distance from, because it was mysterious and subjective, while SFN was more real and could be supported by a biopsy.

I hope one day we will understand how all this fits together.
 
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Creekside said:
I wonder if anyone has checked for muscle activity in resting PWME. I'm imagining some signals causing the muscle cells to contract randomly; enough to qualify as exercise, but not enough firing together to move limbs noticeably.
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This sounds plausible to me from an experience standpoint. In a crash, I sometimes feel like I can’t fully relax my muscles at rest.
 
Hoopoe said:
Re. orexin. It is a neuropeptide. There are over 100 known neuropeptides in the human brain and the expectation is that more will be discovered.

Since they affect so many different things, including sensory perception, regulation of the vascular system, metabolism, sleep, they seem potentially relevant to ME/CFS. I remember leptin has come up before in ME/CFS, although this was in relation to its peripheral role.
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Yeah, i always thought is was something damaged in the brain to do with sleep because i have never made much improvement over 20 years. But how the symptom PEM would fit into that is a confusing worry.
 
ME/CFS Science Blog said:
But isn't that a peripheral neuropathy, one that wouldn't explain any of the core ME/CFS symptoms?

And why would a injury that is not severe cause much more debilitating fatigue symptoms than the severe CNS injuries that are already known?
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Yes, I mixed up CNS with neurological in general.
The issue isn't merely the injury, but the response to that injury. Eg nerve sensitisation.

The brain receiving out of wack autonomic or fatigue signals can have explanatory power. The fact that ME/CFS like syndromes are common post-GBS should give pause for thought.

Autopsies of severe ME/CFS patients HAVE revealed DRG neuropathy so it is a viable hypothesis.

EndME said:
What is not quite clear to me about a neurological hypothesis: Why are these problems apparently more common after glandular fever? How does EBV seemingly have more influence on synapses or neurons than other viral infections?

If we accept a comparison to something like a "ongoing sickness response", then I see no reason to also not see a similarity to the PVF that EBV causes in many people, but why is EBV particularly good at doing that?
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This is a good question. EBV and other herpesviruses are known to infect peripheral nerves and can sometimes be found in cerebral-spinal fluid too.

www.frontiersin.org

Frontiers | Epstein-Barr Virus and Neurological Diseases

Epstein-Barr virus (EBV), also known as human herpesvirus 4,is a double-stranded DNA virus that is ubiquitous in 90-95% of the population as a gamma herpesv...
www.frontiersin.org www.frontiersin.org

The herpes viruses and particularly EBV are far more complex than other viruses, having *far* more genes than most viruses at about 85 allowing for much more complex behaviour.

Utsikt said:
Sure, but then they would be very unfamiliar with how ME/CFS patients usually present.

But I have no idea if pwME/CFS have more muscles than other similarly inactive people that can still use the muscles.
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Your body adjusts to the intensity of activity over the week, rather than the quantity. You can easily go backwards in fitness when doing 10,000 steps per day if it reduces your intensity peaks.
 
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