Small Fiber Polyneuropathy (SFPN) Proposed as Cause of Exercise Intolerance In ME/CFS

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andyguitar

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RebeccaRe said:
I would be curious to know what the rate of SFN is in the general population: if you were to grab 100 people at random off the street, how many would have SFN?
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It's about 5 per 10,000. But as @Badpack has pointed out you also need to look at who gets it. So its almost always related to diabetes.
RebeccaRe said:
It is important to note, however, that SFN affected about 40-50% of the ME/CFS or FM patients these doctors described
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Badpack said:
But just like diabetes, it seems more like a problem which develops over time because of the bad circulation and energy state of the body
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I put these quotes together as for what it's worth i think SNF is a result of cfs/me and it might have only been found in 40-50% of the subjects due the the severity and length of their illness. I dont mean this in a negative way as the research may lead to progress in treatments.
 
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Badpack

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@andyguitar which disease in this age has the chance to go untreated over years and become a full blown entity anymore. Cfs is so underresearched, its crazy. I guess if you just wait long enough, every sick Cfs person will develop SFN over time.

Thats why im so sad that the nano needle development moves so incredible slow. If we have something in the blood that reduces our energy production, it may be not the absolute cause for Cfs, but we urgently need to know what it is to prevent follow up diseases just like SFN.
 
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Wishful

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Badpack said:
I guess if you just wait long enough, every sick Cfs person will develop SFN over time.
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No, I don't think so. Some of us don't get the common physical symptoms that accompany ME. I never developed any physical problems I could link to ME, so I would guess that my risk of SFN is the same as the general population, or possibly even less.

I wonder if my blood would show the nanoneedle response. I think it might not, yet I still suffer from mental lethargy and brainfog, and cerebrally-induced PEM.
 
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Wishful

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Alberta
andyguitar said:
I think the problem over the years has been spending to much time and money on "It's a virus" research. But some will say thats still the way to go.
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I think some of the researchers look at the few trials of antivirals that treated (or cured?) some patients, and see that as proof that a virus is the cause of ME. They ignore the other patients that didn't respond to antivirals, which I would say is wrong-headed from a science standpoint. If some patients respond and most don't, a virus is most likely a factor in the severity of ME for some patients, but not a root cause.

The localized ME epidemics--which do suggest an infectious vector--might indicate that a very specific strain of virus could be better at triggering ME, even triggering it in victims that would not trigger on most other infections. It could remain fairly localized because it's not optimized for survival or transmission in the general public. The population might contain a lot more people who could develop ME, but who have higher trigger limits, and thus encounter fewer microbes that can do it. Hmmm, this would mean that a virus with the genes to trigger ME easily and spreads easily is possible. Maybe that nightmare scenario would help get funding now, before the nightmare happens. <To any ME research advocates, feel free to use this nightmare scenario idea> :)
 
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Badpack

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„In one of medicine's more dramatic moments Banting, Best, and Collip went from bed to bed, injecting an entire ward with the new purified Insulin extract. Before they had reached the last dying child, the first few were awakening from their coma, to the joyous exclamations of their families.„

I expect nothing less from SS31, give me my non fissioned mitochondria back!
 
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wigglethemouse

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pattismith said:
@Cort @wigglethemouse
this is just released:

Long-term efficacy of immunoglobulins in small fiber neuropathy related to Sjögren’s syndrome
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@pattismith @Cort These two papers by Jill Schofield are interesting.

The first one is IVIG for SFPN
How We Treat Autoimmune Small Fiber Polyneuropathy with Immunoglobulin Therapy
Schofield J.R.a,b · Chemali K.R.c
https://www.karger.com/Article/FullText/498858

Abstract
Intravenous immunoglobulin therapy is FDA approved for the immune-mediated peripheral nerve disorders Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, and multifocal motor neuropathy.

Immunoglobulin therapy has been used increasingly with significant efficacy in the treatment of patients with disabling autoimmune forms of dysautonomia, which are most often small fiber (autonomic and/or sensory) polyneuropathies.

It is recognized by most who treat these disorders, however, that patients with autonomic dysfunction treated with intravenous immunoglobulin therapy develop aseptic meningitis or severe lingering headache more frequently than other patient populations when this therapy is dosed in the traditional fashion.

We discuss our combined 27 years of experience with the use of immunoglobulin and other immune modulatory therapy in patients with autoimmune small fiber polyneuropathy.
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This second while not about SFPN found that Antiphospholipid antibodies and novel Sjögren antibodies in autoimmune dysautonomia correlate with a high response rate to IVIG.
Intravenous Immunoglobulin Therapy in Refractory Autoimmune Dysautonomias: A Retrospective Analysis of 38 Patients
Schofield JR , Chemali KR .
https://journals.lww.com/americanth...s_Immunoglobulin_Therapy_in_Refractory.2.aspx
Sci-hub : https://sci-hub.se/https://journals...s_Immunoglobulin_Therapy_in_Refractory.2.aspx
Abstract
BACKGROUND: Intravenous immunoglobulin (IVIG) has recognized efficacy in autoimmune peripheral nerve disorders, but there has been limited study of the use of IVIG in autoimmune dysautonomias.

STUDY QUESTION: To determine the efficacy and safety of IVIG in patients with disabling, refractory autoimmune dysautonomias, including patients with postural tachycardia syndrome and gastrointestinal dysmotility.

STUDY DESIGN: Patients with one or more autonomic disorder(s) and persistent serological evidence for autoimmunity who were unable to work or attend school despite usual treatments for dysautonomia were treated with IVIG for at least 3 months at a dose of at least 1 gm/kg monthly.

MEASURES AND OUTCOMES: Outcome measures included the composite autonomic symptom scale 31 survey and a functional ability score.

RESULTS: There were 38 patients, 84% female and mean age of 28.4 years. Of patients, 83.5% improved on IVIG as defined by at least 20% improvement in the composite autonomic symptom scale 31 and/or functional ability score. The mean pretreatment functional ability score was 21% (mostly bedridden), which improved to a mean of 74% (nearing able to return to work/school) for responsive patients after at least 1 year of IVIG. The mean time to the first sign of response was
5.3 weeks. There were no serious adverse events. The Mayo autoimmune dysautonomia panel antibodies and traditional Sjögren antibodies were present in only 13% and 8% of patients, respectively, but antiphospholipid antibodies and novel Sjögren antibodies were present in 76% and 42% of patients, respectively.
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CONCLUSIONS: There is increasing evidence that IVIG is safe and effective in a subset of patients with autonomic disorders and evidence for autoimmunity. A 4-month IVIG trial should be considered in severely affected patients who are refractory to lifestyle and pharmacological therapies. Antiphospholipid antibodies and novel Sjögren antibodies are often present in these patients and correlate with a high response rate to IVIG.
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