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Open access here: www.ahajournals.org/doi/10.1161/JAHA.119.013006 Editorial here: www.ahajournals.org/doi/10.1161/JAHA.119.014084 Funded by Dysautonomia International. From their press release:

Were they not suggesting that it was the combined effect of 1x or more poor performance causes (HV, Mito, Neuropathy) that gave you the different groups? I.e. HV with no Mito/Neuropathy was sub-normal but not SOE. HV+Mito or Mito+Neuropathy etc. was SOE? I understood from other work that the...

It didn't make it clear either way I don't think. The reason I leaned towards the assumption it was retrospective was because of the review type and funding. It's unclear but they cite a CFS diagnostic guideline after saying the patients had diagnosed CFS, then in the next sentence say: 'we...

Some interesting points raised @Snow Leopard. I think some of the confusion/disappointment might stem from this not really being a CFS study? Not much of a structured study at all really. I don't think it was reported correctly by ME/CFS News (above), my interpretation after reading comments...

The exertional intolerance (defined by SOE) here is essentially a measurement of peripheral oxygen extraction. It could be that PEM is a downstream symptom of abnormal SOE. I expect its a lot more nuanced than either of those explanations though!

This paper uses an ME/CFS cohort, but seems to only really consider them as being patients with unexplained exertional intolerance. There is no attempt that I could see to make any conclusions as to the pathophysiology of ME/CFS based on these results, merely that in patients with unexplained...

Agreed. The layperson's interpretation of hyperventilation is unfortunate, using the word scientifically does not infer anything about the cause being related to anxiety. The paper offers several physiological explanations for hyperventilation and the conclusion explicitly states it should not...

Yeah, that's the train of thought from people like Dr Oaklander and others, an antibody interfering with normal activity. They established in a small study of these 'apparent autoimmune' POTS patients that something like 80+% got an awful lot better on IVIG, the damage wasn't permanent. The...

I guess the same underlying mechanism that first damaged/disrupted your sensory small fibre nerves eventually hit the autonomic small fibres too - or perhaps it was 2x separate causes! It does seem quite possible to have just one or both being affected.

Glad you get on with midodrine - unfortunately that one is off limits to me because I lean more towards the hyper adrenergic POTS spectrum, my BP tends to shoot up when upright, so it could be a little dangerous. Very early days with the pyridostigmine, still titrating up from a tiny dose and...

Hi @ProudActivist, Sorry to hear you get these problems too. Out of interest, do you notice a mottling, red/white lacy appearance on your skin? I know this is not a symptom specific to SFN, but I certainly notice it as more obvious when my circulation/ANS is playing up. Some other things that...

Here are a few of the many possible causes to explore, these I can offer from personal experience: 1 - Hyperventilation. This isn't necessarily rapid panicked breathing, it can happen from slow, overly-deep breathing due to experiencing that 'air hunger' feeling. Particularly relevant if...

This may be way off the mark but something I recall from my autonomic workup was a carotid sinus massage to check for carotid sinus hypersensitivity. Before worrying about things like CCI it might be worth considering? I don't know much about it but understand that compression of the carotid...

POTS is a simplified/lazy way of talking about wider autonomic dysfunction and is absolutely not limited to having simple issues that only occur upon standing. It tends to be defined that way because that is the easiest thing to test. Increasingly research is showing there is underlying small...

Hi @philw44, welcome. Your readings and description of symptoms are a very good fit for POTS, which seems to overlap with ME/CFS and is a very common misdiagnosis. The fact that you don't seem to deteriorate despite further exercise on a PEM day makes me wonder if you lean more towards...

I have the same thing, it tends to track with general health and has become more noticeable recently with it often visible on my upper arms, as well as hands and feet. Initially it was only noticeable when standing for long periods or with temperature changes, but now it is pretty consistently...

So the POTS patients studied must have occupied an awkward middle ground of lying down long enough for mechanisms to effect their venous return but not long enough to cause deconditioning of the heart muscle? This seems like a bit of a narrow window to me.

I'm confused - doesn't deconditioning lead to high filling pressures? I thought a key take-away from Systrom's POTS work in 2016 was: cardiac mass was reduced but low filling pressures were found in POTS iCPET - opposite to expectations in deconditioning.

Impedance plethysmography has been used in POTS studies to show the fractional change in regional blood volumes. Its not precise enough to distinguish between thoracic and splanchnic organs though.

Check out Julian M. Stewart's studies. Their group's work has explored cardiac, respiratory & SNS observations in POTS and their order of appearance - they disproved that simple hyperventilation triggered all the other symptoms, for example. They found what you described, that reduced cerebral...