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But still in Sheffield for yesterday's Lancet paper?

We were discussing the more general relevance of POT. In fact EndME set up a new thread as a result of that side discussion. I am being consistent in not referring to the NIH study. Sorry there was a typo in the last post that may have possibly confused. I am talking about the body of studies...

The other thing is that a high proportion of people with ME/CFS have OI yet do not show POT on testing. So there are good reasons to think POT isn't the real problem.

Sorry but that is simply not the case. The arguments I was making made no reference to NIH data. I don't know anything about their POTS data and wouldn't make use of it anyway, considering the other flaws in the study. There is no coherent story that I can see. Either it is preload failure, but...

I wasn't referring to the NIH findings. I was referring to how one makes a coherent physiological story around the implication of POT in ME/CFS. Maybe the problem is that other people have been convinced of what they are going to find without having thought through whether it adds up in terms...

Except that venous pooling with preload failure would indicate failure of vasoconstriction rather than excess vasoconstriction. I guess it might be possible to put all these things together into a single coherent story but I have a strong suspicion that we have what is called an embarras de...

But presumably the same Chris Burton who has co-authored on other occasions with these Aarhus people giving his address as Sheffield. Maybe he moved?

A bit sneaky really?

Is this another Chris Burton - cloned from the one in Sheffield or wherever, or the same one with two addresses? To answer my own question it is the same one, except here with address give as Aarhus. It beggars belief that someone who sat on the NICE Guideline Committee should be turning out...

I understood that POT was defined as in the absence of orthostatic hypotension. I would have thought that the relevant blood pressure was ongoing over a period of many minutes, not immediately after standing, which might easily drop temporarily.

And what evidence do we have for that? And how do we explain the cerebral symptoms with normal blood pressure if that is the case? 'Neurovascular dysregulation' is hand-waving if you don't mind me saying so! I don't see any evidence of autoantibodies. And IVIg is pretty useless at the best of...

Yes, but what would be the mechanism of origin? Why would you get preload failure in the context? Maybe some selective autonomic defect, but as far as I know nobody has suggested what or why. And in a way it cannot simply be preload failure because if that was the cause there should be a fall...

Mycoplasma is an interesting organism because it produces a range of atypical immune reactions. It can produce Reiter's but also the antibody mediated cold-agglutinin phenomenon.

That is an interesting history. I have in my study the small wooden cabinet constructed by John Honor, who was chief technical officer to Thomas Lewis, with drawers labelled 'histamine', 'cannulae', syringes' etc. What I think may be significant is that this group of Civil War soldiers had...

A typical example of how 'lived experience' and 'empowered' are manipulated to justify poor work. And the usual 'multidisciplinary' garbage.

This looks pretty enlightened. I guess that the wording of requests e.g. 'need a list of outcomes, appreciate links' is a reasonable way to encourage everyone to suggest sources of information. In the NICE exercise, though, the initial phase of asking everyone what they thought was largely...

I agree. I was thinking of writing almost exactly the same post. So far nobody seems to have worked out a plausible mechanism of origin for POT. It isn't just autonomic failure. It is very unclear to me where it is supposed to start off. I suspect it may not be a very good way of categorising...

That may be a good analysis. At present I am focusing on the issue of managing OI and potential cerebral hypoperfusion in the context of very severe patients unable to eat and needing nasogastric feeding and trying to put out a viewpoint document on that. It is a problem that has been followed...

I think you may have misunderstood the context of what I said. As indicated to Hutan, I suspect things are complicated. I am quite certain ME/CFS is almost always associated with OI. The discussion of blacking out on standing was in response to Jem's question. I am not sure that it has much to...

That is what I would have predicted, but we don't have good evidence for the changes in cerebral perfusion reported on tilt table tests are actually the primary cause of the OI. SO things can easily get complicated.