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I'm not an expert on this but I'd suggest methods that modulate the excitability of the DRG and/or spinal cord independently via several methods - Dorsal root ganglion stimulation ('placed near the cell nuclei of the afferent neurons of the dorsal root ganglia') or tonic spinal cord...

The frustrating part of the "central sensitisation" narrative is so many people believe it is ABNORMAL, when in fact central sensitisation is a normal part of healthy pain signalling. When invoking central sensitisation as an explanation for pain syndromes, they don't merely have to...

I kind of dislike these studies (in terms of generalisability) because B-cell autoimmune disease is not a generalised loss of tolerance, it's sensitisation to specific antigens which is a qualitatively different phenomena. They start off with mice which have unusual genetics that have altered...

They also lacked knowledge on how to test things properly across numerous sub-studies, the study of TMS excitability was flawed in numerous ways that wouldn't have happened if they actually bothered to read any research written by exercise physiologists in the last 10 years about how to do this...

Yes, COVID has always been very razorblade/throaty!

Especially as most PwME's SES income/status tends to plummet after becoming ill.

That is an excellent point and a key confounder for small convenience samples like this compared to large GWAS studies.

The discussion section where they try to explain what the relevance of these genes are is quite a stretch, due to lack of primary research. (same goes with the link to neuropsychiatric disorders / autism, we simply don't know enough to say this) I want to believe the NBPF and GO:0050773...

This is a great thread. I make music sometimes (it's quite demanding cognitively), but I don't sing because I hate my voice so they aren't ME/CFS related.

Seems like more evidence against the use of SSRIs...

I didn't get fevers even with normal levels of NK cells, so it must be something else at least for me.

I did not have a genuine hot fever for about 20 years (despite many infections), until COVID, but I wonder whether I just had the sub-clinical sort of fever on rare occasions.

I don't think a doctor has ever described me as delightful, though I clearly am, I was peturbed by doctors who say they are 'impressed' by my symptoms.

I do think this can explain a small minority of ME/CFS or ME/CFS-like cases, note that those cases present differently eg with symptoms like tremor etc. But a large majority of patients do not have this problem.

I think we need to study that explicitly before forming any conclusions. It's not a universal experience but I'm sure some on this forum attest to it. Most people naturally avoid "rolling PEM" anyway, because it sucks.

Another junk study with zero thought put into the validity of the outcome measures given the lack of blinding. I hate the title "Take charge" and the lack of acknowledgement that de-medicalising a medical condition can cause harm.

I suggest re-reading Engel. Bio-psycho-social was *explicitly* a practise based approach rather than a causative theory. Some may have tried to twist it towards the latter in the years since but the evidence has never been there.

Pacing doesn't really lead to improvement of functioning over time though, it just allows some people to carefully do something (within their limits) rather than nothing.

Irritability in particular for me is a big warning sign!

In my experience, I find the 'sleep reversal' is due to a mismatch in the amount of waking versus sleeping hours that the body demands. It means the sleep-wake cycle becomes out of sync with the 24 hour cycle. Napping can increase this risk too but sometimes you just must nap.