Do you still believe that EDS has no connection whatsoever to what is known as ME/CFS? Meaning EDS has the same prevalance rate in HC and ME/CFS?
I have every reason to think this is the case. The suggestions of an association look to me highly unreliable.
Could you please define exactly what is PEM, and how it differs from fatigue (that has been triggered by exertion) in other diseases?
What is this PEM that so many seem to bet their horses on? And if you can not explain it to me in scientific terms and or studies to proof how it differs between ME/CFS and lets say primary mitochondrial disease why would you use it as an exclusion criteria for other diseases that might be causing the very symptom?
PEM involves a worsening of symptoms over a time frame that does not fit with simple exhaustion of energy supply at the time or even with the normal fatiguing that occurs after a period of hard exertion (having had enough of hiking by tea time). It is characteristically delayed (i.e. it hits the person later after a period of being OK) and prolonged - going on for days, weeks or more. There is no other illness where I have reason to think this occurs, with the possible exception of the fatigue associated with autoantibodies like Ro, where it is hard to be sure PEM is not a feature. In conditions like mitochondrial disease where we have some understanding of mechanism PEM would not be expected from the mechanism (and as far asI know does not occur).
Would you say that POTS and other dysautonomia symptoms are part of what is known as ME/CFS?
People with ME have orthostatic intolerance but whether this is related to postural tachycardia or dysautonomia I am very uncertain.
Would you say that symptoms of dysautonomia are more prevalent in EDS and ME/CFS than in healthy control?
I think that can be a misleading question. A lot of symptoms crop up in many conditions. The diagnostician makes use of combinations of symptoms and their patterns to make a diagnosis. So symptom overlap is everywhere, but that does not tell us much.
How would you define the set of symptoms that are related to brain stem and cord compression?
Would you not think that there is a difference between chronic compression (bone structure issues causing vertical instability i.e) and non chronic (in that it is non constant in nature) repetitive shear and tear that is caused by hypermobility of ligamentous structures?
Weakness and numbness in the arms, stiffness in the legs and unsteadiness, sometimes problems with swallowing or facial sensation, problems with bladder control of a specific type. There are many but the combination of features should be reasonably easy to interpret.
I do not know what you mean by vertical instability - things do not move up and down where neck meets skull, only back and forth.
I don't think we are talking about shear and tear. If you actually tear the spinal cord you are likely to die immediately.
I agree that there are different situations though and these tend to be reflected in the symptoms. Intermittent compression can produce blackouts. Chronic compression produces gradually worsening numbness and weakness.
Who are the experts that you are stating? Can you name them?
I think I have mentioned names where specific I have quoted specific points. Otherwise I am going on the basis of what I have read and heard at presentations and from colleagues I worked with over years.
How would you diagnose a cervical instability that is caused by ligamentous instability if not by comparison of flexion and extension of the neck (the chance that this (being lax ligaments in the neck) is not happening to people is 0%)
As indicated in the review from Liverpool we are not interested in 'instability' so much as movement that is sufficient to cause compression. So a clear diagnosis is based on showing compression, not just movement. Excessive range of movement on x-ray or scan might make one suspect compression could be occurring and one might monitor clinical signs and scans. But the detail of how one would manage the case would be very dependent on all sorts of other factors including the underlying cause and I would decide in discussion with a neurosurgeon if necessary. I am no longer practicing so there is no particular neurosurgeon I am thinking of. I think both of us would be aware that the literature on benefit from surgery is very sparse and inconclusive so a sensible judgment would be made on each case hopefully.
Further, how would such knowledge be established (that there is cci and aai that can only be diagnosed with uNRI) if there are no ways (do you know the number of uMRI in the world) to test the hypotheses? What is the chance that diseases that have close to zero research (being ME/CFS and or/EDS) would be deemed necessary to look into when a decision is made whether or not uMRI is needed for the general population?
That is simple. The neurosurgeons should have been doing organised prospective studies over the last forty odd years recruiting all their cases if possible to trials. That is what the oncologists have always done with their patients and that is why treatment of cancer has advanced so much. It requires a degree of humility on the part of surgeons to accept that they might not know best and also taking the time to do long term follow up.
To take „there is no research“ as an argument in (a) disease(s) that are notouriously neglected seems not very wise at best.
It is not an 'argument'. It is, as you clearly agree, a fact. And if past experience is that a significant proportion of people receiving a treatment die on the operating table or within a week or suffer complications in the long term then it seems unwise to consider it for a condition that shows no signs of being likely to benefit, having no similarity in clinical picture.
