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

chillier said:
I think we shouldn't exclude the possibility that there is damage occurring, a few reasons why:

1) As has been alluded to ME/CFS like fatigue is also seen in CNS injury:
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Concussion fatigue is caused by the brain immune activation rather than the injury itself. Though it's possible that ME/CFS could be caused by similar injury, it's more likely that the brain immune activation is responsible.

I'm not sure if concussion fatigue patients suffer from PEM either. I don't mean rapid fatiguability which make them more tired than healthy people for the same amount of exertion. I mean by PEM the bottom falling out when crossing the threshold of exertion.
 
poetinsf said:
Concussion fatigue is caused by the brain immune activation rather than the injury itself. Though it's possible that ME/CFS could be caused by similar injury, it's more likely that the brain immune activation is responsible.

I'm not sure if concussion fatigue patients suffer from PEM either. I don't mean rapid fatiguability which make them more tired than healthy people for the same amount of exertion. I mean by PEM the bottom falling out when crossing the threshold of exertion.
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Many people with post-concussion syndrome suffer from something akin to PEM and I don't think anybody has any idea on what the cause of post-concussion syndrome is.
 
jnmaciuch said:
I definitely understand your desire to prioritize the neurological angle, but I’ve had some discussions with coworkers and classmates with more of a neuroscience focus over the years about this exact possibility and the answers to “what’s the next step if ME/CFS turns out to be in the brain?” have left me pretty disappointed. It’s far off in a way that most other biomedical research isn’t—a fact that I didn’t fully comprehend until I was walked through the limited set of neurological phenomena that could be measured [edit: especially without an animal model] and the even more limited conclusions that could be drawn from any of it. The few examples of successes with migraine and epilepsy are mostly due to the triggering phenomena in both cases being substantially different to the sort of “broken loop” mechanism proposed here.

If it does turn out to be a broken neurological feedback loop, we’d more or less end up in a “throw psychiatric medications at a wall and see what sticks” scenario.
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Yep if it turns out to be a neurological CNS illness that is frankly indistinguishable from being neuropsychiatric we are all well and truly fucked, period. This would be devastating
 
My physio was surprised at how much muscles I’ve got after being bedbound for a year and walking 50m at most a day.

I don’t understand why that would be surprising to them, because it’s what I hear from every single severe (not extreme) patient: I can do it, but the consequences of doing it are bad.
 
EndME said:
I think it's suprising because one might expect more muscle wastage from inactivity. That's independent of whether one can do something or not with payback.
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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.
 
EndME said:
And that should be surprising? I think most PT's won't knowingly see more than a handful of cases in their time (in the UK there's approx 400 000 ME/CFS cases and 40 000 PTs).
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Sorry, I completely forgot to add the context: the person works almost exclusively with pwME/CFS.

I agree that the average physio probably has no or little contact with severe pwME/CFS.
 
BrokenBeaktheBrave said:
He was shocked to hear that I spend most of my time sedentary given the state of my muscle mass.
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I have had a number of assessments by various clinicians, including physios, over the years and more than one has noted that I do not lack core strength or muscle mass, plus basic reflexes, coordination, etc.

How does this fit into the critical deconditioning part of the psycho-behavioural model?

The blindingly obvious answer being, of course, is not only that it doesn't, it in fact directly contradicts it.

I think one of the big under-appreciated clues in ME/CFS is that we are not more deconditioned. If it was a central feature of the disorder then it should be obvious, much more obvious.

Yet it just isn't there in the vast majority of patients. Very severe, completely bed-ridden, long-term cases being the exception that proves the rule.
 
If 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?
 
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.
 
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