I remember seeing at least one paper showing an ion channelopathy in ME/CFS. But it is one thing observing a pathophysiology like this, but quite another to connect it to specific symptoms.
Do you mean that there was a paper showing that an ion channelopathy exists in ME/CFS but that they were not able to link it to specific symptoms (like muscle weakness, etc)?
They do mention ion channel issues in ME/CFS in the original ICC published paper, but the original published paper does not mention ions in the title of section D. So it could be a mistake, but I am not sure.
That is all very strange and I have no idea how to interpret any of it?!
I think the explanations about what’s going on are way too obscure. Occam’s razor- ME is an infectious, inflammatory nervous system disease.
Do you think (for a sub-group) that it could start out infectious and then flip into autoimmunity?
Many of us have similar patch-work diagnoses stories to tell, don't we?
We have Chinese Menu diagnostic protocols, with lousy fortune cookies.
Yes... that is definitely a good description!
There are often two elements at play here, and these may be more peculiur to her channelopathy. There is the defective ion transport mechanism which translates immediately into poor muscle stamina etc. But, there is also the downstream cardiac issues which feed and compound the weakness and exhaustion.
My understanding of the calcium channelopathies are that they cause muscle weakness, that can be severe and affect the lungs/diaphragm and breathing like in my case prior to treatment, but I haven't heard of them causing cardiac issues. BUT this just may not be known yet since almost 100% of the people in the calcium autoantibody group that I belong to also have POTS.
I think it is exciting that IVIG and Rituximab helped you. I love to hear successful treatment protocols. But you still have symptoms, yes?
I have been really been agonizing lately over how to best describe my current situation and feel like the best description is "partial remission". I will never use the word "recovery" or "cure" re: my case b/c when I stop Rituximab, all of my disabling symptoms could return. In addition, I still take several other meds, I still do not have the muscle stamina that I did pre-illness, and I still cannot climb stairs.
So if "remission" means "pre-illness level" than it is not the right term for me. But I have vast improvement (my breathing is now normal, I can stand, walk without wheelchair, drive, no allergic reactions to food, etc). I continue to strive toward what I would call a full remission but not sure if I will get there (and I don't at all mean that as a complaint and am beyond grateful for my current state, I just wish it could improve a little bit more).
I am facsinated by this. IVIG rebooted your system. No problems since? Of course, this suggests acquired, and I know you know this, but maybe not, right? It still might be genetic? Or you are certain it is autoimmune? Either way, your story is so hopeful that I get a lift inside each time I read your posts.
IVIG re-booted my immune system so I was no longer allergic to food and no longer had anaphylaxis (since 2016). It caused several other improvements but I was not able to walk without a wheelchair and have normal breathing/muscles until Rituximab. The two worked in conjunction with each other in my case. My doctors feel my autoimmunity is acquired BUT it makes sense that I also had some kind of genetic predisposition b/c other people have had my set of triggers (neurotoxic reaction to a med, severe Mono/EBV, and toxic mold exposure) and been able to recover vs. I was not and continued to progressively worsen prior to treatment.
I mean "they" have only begun to scratch the surface of even qualifying the channelopathies they've discovered so far, and I strongly suspect more discoveries will be coming. Which means more investments into more and better tests to capture diagnoses - covering the spectrum of diagnostics - quicker and more definitively.
I agree.
I'm just not confident about the time frame. I want to believe sooner than later, but history doesn't necessarily support that.
I am not confident about the time frame either
First muscle issues were in the upper legs
Everything that I read about LEMS says that the upper leg muscles are the first to weaken but this did not happen in my case which makes me question the diagnosis. My legs never weakened and it was all my upper body (arms, neck, lungs, diaphragm, etc).
I think it is a shame that one of the main criterium for LEMS is "getting stronger with exertion" (although I seem to remember that it was some strength gain after 10min, and then a weakening) and most LENS people then say, "Well no, my muscles get weaker". There's something really wrong. I do wonder how pravelent this is, which practically means worse diagnostics (i.e. more misdiagnoses).
I'm sure it must vary greatly for each person but in the group that I participated in, many people said that their muscle weakness was progressive and exertion was not possible and certainly did not strengthen their muscles. I wish I knew if it really was my diagnosis.
I didn't know it's linked to general autoimmunity. Shows I need to search more about it. Thanks !
Anti GAD65 definitely links to general autoimmunity (especially in cases where the person does not have diabetes or Stiff Person Syndrome).
Thank you
@Hip and I bookmarked this to read later. It is very possible that I have already read it at some point between 2016 and now but do not remember