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Those pictures look pretty normal to e. This is my hand resting on the arm of my chair.

I am sceptical of that. GPs were taught to diagnose primary hyperparathyroidism by asking for a 'bone profile' of calcium, phosphate and alkaline phosphatase fifty years ago without most of them remembering why those tests were useful. Maybe wariness of black box sets of results where none of...

This is where it all gets so hard to judge. I don't think autonomic failure would lead to valve failure. A proportion of people have valve failure - I guess a big enough proportion for quite a few people with ME/CFS to have it by chance. I wouldn't be surprised if the effects of OI on daytime...

But hang on. Do you actually mean co-morbidities? Because something is only a com-morbidity if you have already diagnosed ME/CFS and are looking for something else as well. Hypertension is not a problem because you diagnose it by taking the blood pressure and always will be. Hypothyroidism is...

But is this real medicine? Have you had experience of how this actually works in clinical practice? Because it doesn't work the way most doctors assume it does. We don't even know what we mean by a 'more accurate diagnosis'. We think that a group of people have a common element to the mechanism...

What is needed is not further research but a little bit of common sense and understanding of human nature and medical ignorance.

I am pretty sure that any diagnostic procedure that does not provide information on mechanism will only ever be circular. Its validity is based on correlation with the uncertain clinical classification you want to do better than, but it will only ever be second best to that. Jobbing doctors and...

Right. I think that was what I was saying.

It all sounds very sensible but does it actually provide any useful guidance. There is still a talk of multidisciplinary care - without any reason being given. It would be nice to have therapies but what is 'therapeutics-focused research'? In my experience it is doing the biology first so that...

I think most of us on the forum would agree with that question. To my mind things like Hoover's sign simply indicate that the problem is at a higher level of processing than can be analysed by the traditional neurological examination. It also begs the question of what is meant by FND. The FND...

We know that different neurons have these different tasks and on an informational basis it only makes sense for those that compute the difference from expectation to be different (upstream) from those that are informed of that difference and experience it. There is of course no 'we' in...

So many things are claimed to be commoner in ME/CFS when it seems likely they are not that I think there is a need to be cautious. I have just got out of bed and stood by the wash basin for three minutes and my leg veins are bulging. I have quite extensive denervation of my feet from sciatic...

That seems to have become the folklore amongst ME/CFS physicians but I am not aware of any scientific evidence base for it and it doesn't seem very plausible from first principles. So much of this stuff is folklore rather than physiology. It has been suggested that people with ME/CFS have low...

Those quotes suggest the usual sort of confusion over the precise dynamics that you get if you treat the brain as a 'system' and try to make events non-local (as this does). It tries hard to dissociate 'agency' and 'control' from consciousness but is bound to fail if it tries to explain in this...

Just for fun I asked Google, who said: Yes, gamma interferon (IFN-g) is produced during innate immune responses. While primarily associated with adaptive immunity (Th1 cells), early production of IFN-γ is a key part of the innate defense, acting as a bridge between innate and adaptive systems. !

Absolutely, not to mention the PACE trial showing that you can make people at least say they are better but they turn out objectively to be the same. If this is just a re-run of ME symptoms just being believing you have ME symptoms we can pass on.

The thesis astract is pretty vague. I am not clear what is meant by a Bayesian framework here. He points out that what he proposes is in contradiction to the active inference prediction and error detection model used by those who study specific senses like vision. The basic idea seems to be...

I agree. I don't think concepts like 'central overload' have any useful basis. I don't think we have an neural data to ink it to and the concept itself seems confused. Is it overload if it is a normal input that is being responded to differently? If it is defined by the adverse response then...

That applies to true autonomic nervous failure, as in multi-system atrophy. But there is no particular reason to think it applies in ME/CFS.

I am not distinguishing any of these. Just something that leads to a later change.