Jonathan Edwards
Senior Member (Voting Rights)
There aren't that many of us anywhere, but there were several in the US long before me. (I had no private income. I just made use of some of my government salary.) And there are enough of us to constitute a fairly major proportion of innovation in chronic disease treatment. The drug companies just come in to do the second generation stuff.
I suspect much of the problem is simply that medicine has been taken over by greed like everything else in the last forty years. And no intelligent youngster goes in to medicine if they can make it rich in finance.
And what sort of doctor is that? Too busy handing out stuff they don't know if it even works.
I actually have seen it, and it turned out exactly like you said – not very rigorous. Dr. Luke Liu in Anchorage did a trial on stellate ganglion blocks for ME/LC/something like that, and he didn’t blind it. When I was there, we argued a lot about it – he said it was impossible to do, I said it was difficult but not impossible and gave him some ideas for how to do it. Ultimately he decided not to blind it. I don’t know what his clinic’s finances are like so I don’t want to cast aspersions. I do know he gave away a ton of free treatment and that probably consumed significant resources and made it difficult to carry the trial out as I suggested. Essentially I suggested two things – 1) add a third arm with a pill-based treatment so that everybody would get some pill to take and the ones receiving the sham SGB could at least wonder whether they got the treatment pill (LDN, one of those OTC blood thinners that were popular for a time among patients who thought they had microclots, whatever), and 2) isolate the patients after the SGB in a room for a few hours without a mirror or a phone so they couldn’t look at themselves and see whether they had the Horner’s reaction. Both would have required a lot more resources.
Trials have gotten really expensive to run with all of the reporting requirements.
PEM isn't simply "more intense fatigue after more intense exertion".
The exhaustion is out of all proportion to the effort. It's often delayed, involves multiple symptoms like the sickness/flu-like feeling, muscle or other pain, fatigue and worsening of other symptoms and lasts for a long time.
Like I mentioned before, autoimmune diseases among other symptoms also present in ME like fatigue, can have post exertional symptom exerbation, which as a difference to PEM isn't delayed, mostly not that long lasting and has a lesser amount of different symptoms.
I didn't want to attack you or to invalidate your experience, what I wanted to ask is if you can be sure that you didn't experienced those symptoms due to the autoimmune neuropathy BEFORE your symptoms of orthostatic intolerance occurred.
But that's not my point, my point is you can't claim that IVIG helped your ME if you have autoantibodies indicating autoimmune neuropathy, an illness where there is (low-grade) evidence that IVIG may help.
And I'd argue that at least in your case with positive autoantibodies against TS-HDS in the blood, you can't make the argument that it's maybe the same as ME, I am pretty sure we would know by now if this was something that is really common in pwME. Afaik it isn't exactly a routine test, but after all Flugge/Mella and especially Scheibenbogen have searched for all sorts of autoantibodies in the blood of their ME patients for years and I sincerely hope and believe they would have noticed this.
Like I said my biggest takeaway from your story is the importance of looking for possibly treatable comorbidities and I am really glad you had the opportunity to find one and treat it.
Yes that would have been smart and you were definitely right in your arguing with him. Also he could at least have a waiting group or a 'usual care' control, because many people recover in their first year of Long Covid.
Among small case studies of 2-3 people the only bigger study he has published to date on Long Covid is this retrospective one with 33 participants:
https://www.sciencedirect.com/science/article/pii/S1566070224000493
And my problem would be less with the study itself, it's understandable if he has no money there, but with what he makes of it.
Of 33 persons 10 were deemed as long term responder (1 month). He excluded persons with pre-existing ME, POTS as well as fibromyalgia. He did no personal follow-up except for the questionnaires at 1 months.
The problem is despite these in my humble opinion, sobering results, he went on the public Stanford symposium for ME and declared it a promising treatment. One thing is the mediocre result in Long Covid patients, another thing is the presentation of this treatment at an ME conference when having absolutely no data about it in this illness.
I had those things! Muscle aches in parts of my body that I did not exercise. Headaches, sore throats, and brain fog that came on within a day or so delay after exercise. Sorry that I did not list exhaustively every symptom that I had in my original post. Fatigue was the most debilitating, so that's what I focused on. But I also had the more unique-to-ME things. It was already getting very long and I blocked out that part of my life because it was so painful. Another thing, to be honest, that I blocked out was the dynamics of these online patient communities, and the skepticism that mild people encounter that they were ever really sick. But yes, I had these symptoms.
I can't be sure, and neither can you or anybody else, because none of these diseases are well researched, diagnosed, or even diagnosable enough. Autonomic neuropathy is not even directly observable when a patient is alive, because you can't biopsy autonomic nerve fibers without killing somebody and dissecting them. You can only infer it indirectly through a skin punch biopsy, which analyzes sensory nerve fibers, which are related to autonomic nerve fibers in that they're peripheral but are a bit different as I understand. And by the way, my skin bunch biopsy came back borderline negative – the neurologist had to make the case that I had it due to my age (like, it was within the reference range, but she found some study suggesting that the reference range was overly conservative for somebody in their 30s). And I asked later if we should redo it and she basically said no, these tests aren't that reliable anyway, the only purpose was to get insurance approval and now that we have it, we don't want to risk doing it again and it being negative. Just to give you an idea of how unsettled the science around SFN is.
I wrote my post to try to avoid making strong causal assertions. If you reread it, you'll see that I state the sequence of events. It's impossible to not come up with causal theories about your own life, so yes, I think it was critical to the recovery, but nobody's story is ever going to be that convincing. There's just no way around the fact that you have to run a RCT and/or have a deep biological understanding that we don't have.
As for low-grade evidence that IVIg may help SFN – it's so low-grade that there's a consensus statement advising against it, in fact! Insurers and doctors have somehow been friendlier to prescribing IVIg to people with immune-mediated SFN, but I think you're taking that fact and making an unwarranted leap about the evidence base. I don't think the evidence that IVIg helps SFN is that much stronger (if at all stronger!) than the evidence that IVIg helps ME/CFS. I think the reason there's more friendliness among insurers and neurologists to prescribing IVIg is because there's a bit stronger of a basis for diagnosing SFN. But as far as I know, there's no RCT, just a bunch of case studies – which we actually also have for ME!
As for evidence of SFN undercutting an ME diagnosis – tons of ME-diagnosed patients have this! Same with ME-diagnosed patients and POTS diagnoses.
I actually took two autoantibody tests. The first time, with CellTrend, it was positive for TS-HDS and negative for FGFR3. The second time, with WUSTL, it was the opposite. Which is to say, these autoantibodies are fickle and not indicative of much other than that an insurer might approve IVIg for you. The neurologist I have dealt with have been pretty clear that none of this is well understood and all of this is a bit of a game with an insurer. So I disagree with your pretty categorical assumptions of what this all means – that I definitely have SFN, that other people with ME definitely don't, etc.
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