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Dysautonomia and small fiber neuropathy in post-COVID condition and Chronic Fatigue Syndrome, (Azcue et al 2023)

Murph

Murph

:)
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1,799
https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-023-04678-3

J Transl Med
2023 Nov 15;21(1):814.
doi: 10.1186/s12967-023-04678-3.

Dysautonomia and small fiber neuropathy in post-COVID condition and Chronic Fatigue Syndrome​

Abstract​

Background​

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and post-COVID condition can present similarities such as fatigue, brain fog, autonomic and neuropathic symptoms.

Methods​

The study included 87 patients with post-COVID condition, 50 patients with ME/CFS, and 50 healthy controls (HC). The hemodynamic autonomic function was evaluated using the deep breathing technique, Valsalva maneuver, and Tilt test. The presence of autonomic and sensory small fiber neuropathy (SFN) was assessed with the Sudoscan and with heat and cold evoked potentials, respectively. Finally, a complete neuropsychological evaluation was performed. The objective of this study was to analyze and compare the autonomic and neuropathic symptoms in post-COVID condition with ME/CFS, and HC, as well as, analyze the relationship of these symptoms with cognition and fatigue.

Results​

Statistically significant differences were found between groups in heart rate using the Kruskal–Wallis test (H), with ME/CFS group presenting the highest (H = 18.3; p ≤ .001). The Postural Orthostatic Tachycardia Syndrome (POTS), and pathological values in palms on the Sudoscan were found in 31% and 34% of ME/CFS, and 13.8% and 19.5% of post-COVID patients, respectively. Concerning evoked potentials, statistically significant differences were found in response latency to heat stimuli between groups (H = 23.6; p ≤ .01). Latency was highest in ME/CFS, and lowest in HC. Regarding cognition, lower parasympathetic activation was associated with worse cognitive performance.

Conclusions​

Both syndromes were characterized by inappropriate tachycardia at rest, with a high percentage of patients with POTS. The prolonged latencies for heat stimuli suggested damage to unmyelinated fibers. The higher proportion of patients with pathological results for upper extremities on the Sudoscan suggested a non-length-dependent SFN.

https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-023-04678-3
 
Murph

Murph

:)
Messages
1,799
New paper.

Couple of interesting parts.
1. They find a very statsitically significant difference in response to heat in the small fibres. I've often thought heat could be a signal the body is responding to in moments of exercise, perceiving it as excessive and calling it a crisis. I'm not 100% sure how this links because I've never really read up on small fibre neuropathy but this paper has found a big something there. (And heat responses are a small but important part of the whole edifice: https://me-pedia.org/wiki/Heat_shock_protein)
2. They find depressive symptoms are a good way of sorting out mecfs people from non-mecfs people, which is rare. But I'm not going to be surprised if there's overlap in the mechanisms between the two conditions. Maybe depression is just mecfs limited to the brain only?! just japes but still interesting.
 
Murph

Murph

:)
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1,799
While we're speakin about heat and mecfs, I want to mention this paper that found heat shock protein upregulated in Sjogrens pateints with fatigue.

Heat shock proteins and chronic fatigue in primary Sjögren's syndrome​


Kjetil Bårdsen 1 , Mari Mæland Nilsen 2 , Jan Terje Kvaløy 3 , Katrine Brække Norheim 4 , Grete Jonsson 5 , Roald Omdal 6

Abstract​


Fatigue occurs frequently in patients with cancer, neurological diseases and chronic inflammatory diseases, but the biological mechanisms that lead to and regulate fatigue are largely unknown. When the innate immune system is activated, heat shock proteins (HSPs) are produced to protect cells. Some extracellular HSPs appear to recognize cellular targets in the brain, and we hypothesize that fatigue may be generated by specific HSPs signalling through neuronal or glial cells in the central nervous system. From a cohort of patients with primary Sjögren's syndrome, 20 patients with high and 20 patients with low fatigue were selected.

Fatigue was evaluated with a fatigue visual analogue scale. Plasma concentrations of HSP32, HSP60, HSP72 and HSP90α were measured and analysed to determine if there were associations with the level of fatigue. Plasma concentrations of HSP90α were significantly higher in patients with high fatigue compared with those with low fatigue, and there was a tendency to higher concentrations of HSP72 in patients with high fatigue compared with patients with low fatigue. There were no differences in concentrations of HSP32 and HSP60 between the high- and low-fatigue groups. Thus, extracellular HSPs, particularly HSP90α, may signal fatigue in chronic inflammation. This supports the hypothesis that fatigue is generated by cellular defence mechanisms.

--
The good news is our well-funded friends in cancer research have a drug that suppresses hsp90, called onalespib.
https://pubmed.ncbi.nlm.nih.gov/?term=onalespib
Maybe one day we get a case report of a person being treated for cancer with onalespib who has an mecfs remission and some research flows from there!
 
Rufous McKinney

Rufous McKinney

Senior Member
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13,389
Murph said:
They find depressive symptoms are a good way of sorting out mecfs people from non-mecfs people
Click to expand...

I was (not surprisingly) skeptical of this "depressive symptoms" part.

I'm not in a position to analyze the details here, but I will remain skeptical.

Post covid- nobody can have been sick since more than Jan 2020. (ok maybe 5 people got COVID before Jan)

ME CFS: I'm on year 69 of my 70 year saga of unwellness. My ME got real bad: seven years ago.

Things that got me concerned:

- "Neuropsychological and neuropsychiatric evaluations were performed by experienced neuropsychologists"

I would not trust these folks to set aside their neuropsyche biases.

- "anxious-depressive symptoms"

Those symptoms labeled as anxious or depressed, are also the symptoms triggered by Sickness Behavior, unwellness, and not having enough mitochondria operating correctly to run the show (or WHATEVER it is).

How about including an analysis of boredom in these studies. We are also very BORED. People are isolated, and can't read a book (vision too blurred). I can't watch a movie during the daytime it crashes me. So I won't go to a matinee, either.

Thats depressing. Its BORING.

Shall we pass out pills for boring?
 
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