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Has anybody looked into CCI's effect on vagal Ganglia nerve? Or Intracranial pressure on neuroimmune system? Feel free to point me to them. We are not going to have any confirmation till we look. And you can't say there were no neurological problems beforehand since we don't know if ME/CFS is...

You are taking the clinical view while I'm suggesting research. I don't think anybody in their right mind would suggest CCI surgery as a solution for ME/CFS. But exceptional cases often shed light on intractable diseases, and I suspect will be the case for ME/CFS research which has been forever...

I didn't mean all CCI cases present ME/CFS symptoms. But there are a few documented cases of recovering after CCI surgery from what they thought was ME/CFS. Were they coincidences? Maybe. Having a few makes it worth looking into those cases though. Since the paper implicates vagal ganglia nerve...

It's a formal diagnosis as far as I know. I got it when I complained of popping and crackling. The tube got narrowed after an infection and it no longer equalizes the pressure efficiently.

Discussion moved from this thread: A body–brain circuit that regulates body inflammatory responses 2024 Jin et al I wonder if the CCI cases imitating ME/CFS was caused by compressing or stretching vagal ganglia nerve (signal malfunction), while true ME/CFS cases are caused by hypersensitivity...

Eustachian tube is the passage between the middle ear and nose. The narrow passage amplifies the ear pressure during PEM and make the problem much more noticeable in my case.

It could still be useful if we are moving from the diagnosis of exclusion, which often takes years, to a positivity test that takes days. This particular test, however, smells like a marketing job. For all we know, they might have had exactly the same result if they mixed ME/CFS cases with flu...

Such speculation is useless unless you can identify that subgroup somehow. Then you could run the trial again only on that subgroup to validate the theory. Otherwise, it's no different than saying that anything is possible. And that is how some people try to get away with failed trial.

The problem with post-COVID, long-COVID, PASC, etc is that it means anything left over from COVID. If you have anosmia after COVID, you have post-COVID. The trial has nothing to do with overactive immune system. It only means it improved PASC patients' T cell memory or whatever, however they...

Some people seem to have success controlling PEM by keeping HR under certain rate, like 95, all the time. The problem with HR, however, is that it soothes out step function. Do squat, for example, HR will rise slightly and then fall back over a period of a minute or so when squat itself last...

Anything with norepinephrine and dopamine catches my attention. But the result barely clearing the threshold at the last minute in such a small sample size is not too credible. I sure would like to see larger trial for longer with something more objective than FSI (either step count or time...

I just remembered Hornig et al published a paper some 10 years ago stating that the inflammation level does not predict the symptom severity and that immune system goes from hyperactive to hypoactive at around 3-year mark. I wonder how they square the current paper with that one.

I'm probably seeing what I want to see, but if ENS glia can become hypersensitive following acute inflammation, CNS glial cells could as well.

Replace overactive with hyperactive, and Jay Levy said exactly same thing 40 years ago. Too bad he walked away from ME/CFS because of the controversies. If innate PBMC are found overactive, it is not unreasonable to extrapolate that innate neuroimmune cells are also overactive. I think that's...

His team already made the imaging for FMS available. I suspect the ME/CFS study will be similar, except that it'll get wider scrutiny given the controversy around ME/CFS and LC.

I think the point was to simulate the immune system activation without actual infection using LPS to show how ME/CFS feels. The theory is that over-active immune system is making us feel sick. The tracers bind to activated microglial cells as far as I know. So, the tracers lighting up the image...

"Inflammation" in ME/CFS context only means neuroimmune activation, and the subsequent flooding of pro-inflammatory cytokines, rather than the actual swelling of the brain. You can fault people conflating the terms, but you well know swelling is not what they meant.

So, there is a way to simulate immune/microglial activation and ME/CFS fatigue. I wonder if there is a way to simulate PEM. Chronic activation means chronic fatigue, but PEM may require acute activation on top of the chronic one. I suppose you could simulate it by giving more dose of endotoxin...

Thanks, I'm glad you have a better memory than mine. It appears we both have been very consistent on this topic!

Neuroimmune activation in TBS is a rather well-established fact. One could question whether that is the cause of post-concussion fatigue. But neuroimmune activation is also a rather well established as a cause of fatigue, such as age-related fatigue...