It depends on what you mean by electrophysiology, you can't easily probe what we're talking about with needles. You can block the signals in the spine and measure different responses in the brain and if it is muscle afferents we are talking about, we can also measure the differential effect on...
The answer to the general question of nerve sensitisation post-damage, either the nerve endings or in the DRG is yes and it doesn't require nerve crush like the cheap and dirty animal models you see published (the 'damage' stimulus can be milder). I am trying to write about this right now. This...
Interferons (of several stripes) like other cytokines don't cause sensory signals directly, but there are lots of studies showing they can sensitise neurons including in the DRG. (and I will be including discussion of this in the manuscript I am writing that may or may not ever be finished)
Do the T-cells become resident in those tissues, is that why we don't consistently see interferon gamma turning up in cytokine studies?
The Lipkin study (10.1126/sciadv.1400121) found higher levels in the early group, but lower interferon gamma than in controls for the >3 year illness group so...
I still don't understand how the hypothesis is relevant to ME/CFS symptoms.
Is it the FcγRI binding IgG that is relevant in which tissues? How does this mediate ME/CFS symptoms? Do we only have the DRG hypothesis mentioned in the other thread?
And you are suggesting that Rituximab treatment...
It could be, I have heard others say the same thing. There is also an often overlooked relapse-remitting pattern in some patients in the initial stages (where the remission may still not be 100%) and this unfortunately does lead to spurious claims of people being cured (by whatever they were...
Same, it's not the angle I would take, but I think each advocate needs to follow their own ends. I don't agree with the idea that every activist/advocate has to have the same ideas and points of view, there is room under a broad tent.
Syndrome is used when there is a lack of specificity.
An example is Guillain Barre Syndrome. Each case is clearly a disease, but it is not a single disease and most neurologists aren't smart enough to tell the difference so it's still a syndrome.
I cannot stand the Kurzgesagt book, too many errors and misinformation in the autoimmunity section in particular. I think wikipedia is more accurate and valuable to learn from.
I've been exercising on and off for years, my cardiovascular fitness is average/good but brain fog and other fatigue is worse than ever and exercise is what induces OI for me.
It's only an excitatory effect, so it still requires regular afferent signalling for nociception. It remains to be seen if other afferent sensory pathways are affected.
We'd have additional signs if there was ammonia accumulation in the brain and that evidence is lacking.
Ammonia easily crosses the blood-brain barrier so there would be higher levels in circulation as well.
https://my.clevelandclinic.org/health/diseases/24065-hyperammonemia
Anecdotes from strangers don't deserve anything. They could be a tiny proportion of people whom recovered naturally/due to other reasons.
Only people we know personally deserve to be believed.
I've noticed a huge difference in recovery/remission stories (over 25+ years) between those who've...
I don't know either, there are 3 main ones:
FcγRI (CD64)
FcαRI (CD89)
FcεRI
https://en.wikipedia.org/wiki/Fc_receptor
Probably the former, but we'll need the manuscript or JE to clarify.
https://en.wikipedia.org/wiki/CD64_(biology)
I've read this entire thread and I still don't understand how any of this is relevant to the physiology/symptoms of ME/CFS? Maybe @jnmaciuch can enlighten me?
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