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Intriguing. I see nothing in common with ME/CFS except, would you believe it: BTN2A2 and related genes. I wonder if the locus is matched?

Well, we can’t really complain about the bad doctors because they will be replaced by the terrible ones Yes, that I can see. Why does the reply option sometimes not work?

That is the situation that doctors are in. Blow the whistle and you are out sharpish. I am not sure quite how it applies to patients. Patients should complain for all their worth. It won't make things any worse for them as far as I can see.

Good point. Maybe a caveat is that narcolepsy, particularly of the type with cataplexy, is such a unique presentation that one might expect the pathology to be 100% correlating - like myasthenia gravis or polio. If severe ME/CFS is as pathologically homogeneous it would make everything an awful...

No, the general lay public. This is a general issue about governance of medicine. But I am beginning to realise that most of the advocates for people with ME/CFS who get the chance to interact with government are not prepared to challenge lots of things they should. That is how we got to where...

I am not sure we know what this finding actually means in terms of what is happening to the cells. They are not necessarily 'wiped out'.

Does it? Maybe it shows the lack of interest or commitment. When things have gone very badly wrong in some branches of medicine we have had things like the Alder Hey report, the Letby events, the enquiry into cardiac surgeons, the contaminated blood report, etc. All that lay people would need...

That is certainly on an odd looking plot.

By enquiring into what goes on. I could tell a bunch of lay people all sorts of hair-raising stories about unethical behaviour but nobody asks. How come there is still a merit award system for good boys and girls that can double their salary that is almost entirely dependent on networking and...

Yes, that is what I mean. The problem is that people die in all sorts of different ways and the time before autopsy varies. If someone dies of starvation the changes may be very different from dying from a heart attack. And there really aren't that many autopsies done that would be controls...

Probably because there are very few neuropathologists. AI says: UK Context: The British Neuropathological Society has indicated that for adequate coverage, a target of 1 full-time equivalent (FTE) neuropathologist per 1,000,000 population is recommended, which is 0.1 per 100,000. There are only...

Not necessarily. I have seen these problems play out in London decades ago. If you say to the commissioning budget-holders "I think instead of one doctor and forty therapists we she have four doctors and four nurses" you are quite likely to get in reply "We have a better idea. We like to have a...

A study over 10 years seems slow. Maybe there are no more cases to collect but storage and test reroducibility become major issues over that time period.

Except that they didn't find markers of activation. The report of disrupted microglia is odd to me - I don't know how in tissue sections you can tell that glial processes are separated from cell bodies. The author said nobody much had seen this before. I think it would be important to have...

Probably, at least in terms of primary outcomes.

Encephalitis lethargica was post-infective. If the immobility of very severe ME/CFS is neurologically determined there might be other commonalities, but there are major differences.

I know Luis Nacul very well. I think his brief in Canada may have required more of a positive gloss than we would like. The review of practice paper we looked at is quite cautious. Luis takes biomedical explanations seriously and has worked hard with the European ME research network. I would...

From what I hear there was no effect, which, if confirmed in publication, would be quite useful information.

It could but it begs the question why one should suggest that and exactly what would constitute this neuroinflammation. They seem very ready to assume received wisdom before challenging it. Better to assume we just didn't know?

The papers with David are about catatonia and encephalitis lethargica - biological features of brain disease that might well be relevant to ME/CFS.