Myopathy as a cause of fatigue in long-term post-COVID-19 symptoms 2022

[pattismith]

Myopathy as a cause of fatigue in long-term post-COVID-19 symptoms: Evidence of skeletal muscle histopathology​

Eva K. Hejbøl, Thomas Harbo, Jane Agergaard, Line B. Madsen, Thomas H. Pedersen, Lars J. Østergaard, Henning Andersen, Henrik D. Schrøder, Hatice Tankisi
First published: 06 June 2022

https://doi.org/10.1111/ene.15435


Abstract

Background and purpose​

Among post-COVID-19 symptoms, fatigue is reported as one of the most common, even after mild acute infection, and as the cause of fatigue, myopathy diagnosed by electromyography has been proposed in previous reports. This study aimed to explore the histopathological changes in patients with post-COVID-19 fatigue.

Methods​

Sixteen patients (mean age = 46 years) with post-COVID-19 complaints of fatigue, myalgia, or weakness persisting for up to 14 months were included. In all patients, quantitative electromyography and muscle biopsies analyzed with light and electron microscopy were taken.

Results​

Muscle weakness was present in 50% and myopathic electromyography in 75%, and in all patients there were histological changes. Muscle fiber atrophy was found in 38%, and 56% showed indications of fiber regeneration. Mitochondrial changes, comprising loss of cytochrome c oxidase activity, subsarcollemmal accumulation, and/or abnormal cristae, were present in 62%. Inflammation was found in 62%, seen as T lymphocytes and/or muscle fiber human leukocyte antigen ABC expression. In 75%, capillaries were affected, involving basal lamina and cells. In two patients, uncommon amounts of basal lamina were found, not only surrounding muscle fibers but also around nerves and capillaries.

Conclusions​

The wide variety of histological changes in this study suggests that skeletal muscles may be a major target of SARS-CoV-2, causing muscular post-COVID-19 symptoms. The mitochondrial changes, inflammation, and capillary injury in muscle biopsies can cause fatigue in part due to reduced energy supply. Because most patients had mild–moderate acute affection, the new variants that might cause less severe acute disease could still have the ability to cause long-term myopathy.

 

[pattismith]

Myopathy as a cause of Long COVID fatigue: Evidence from quantitative and single fiber EMG and muscle histopathology​

Author links open overlay panelJane Agergaard a, Benjamin Yamin Ali Khan a b, Thomas Engell-Sørensen a, Berit Schiøttz-Christensen a, Lars Østergaard a c, Eva K. Hejbøl d e, Henrik D. Schrøder d, Henning Andersen c f, Jakob Udby Blicher g, Thomas Holm Pedersen h, Thomas Harbo f, Hatice Tankisi b c
MULTICOV Consortium1

2023

Highlights​

• •
  Myopathic changes in qEMG and/or increased jitter in sfEMG were seen in 63% of 84 patients with Long COVID neuromuscular symptoms.
• •
  Low quality of life score correlated with higher mean jitter values in sfEMG but not with qEMG measures.
• •
  Electron microscopy showed damage of terminal nerves and motor endplate.

Abstract​

Objective​

To describe neurophysiological abnormalities in Long COVID and correlate quantitative electromyography (qEMG) and single fiber EMG (sfEMG) results to clinical scores and histopathology.

Methods​

84 patients with non-improving musculoskeletal Long COVID symptoms were examined with qEMG and sfEMG. Muscle biopsies were taken in a subgroup.

Results​

Mean motor unit potential (MUP) duration was decreased in ≥ 1 muscles in 52 % of the patients. Mean jitter was increased in 17 % of the patients in tibialis anterior and 25 % in extensor digitorum communis. Increased jitter was seen with or without myopathic qEMG. Low quality of life score correlated with higher jitter values but not with qEMG measures. In addition to our previously published mitochondrial changes, inflammation, and capillary injury, we show now in muscle biopsies damage of terminal nerves and motor endplate with abundant basal lamina material. At the endplate, axons were present but no vesicle containing terminals. The post-synaptic cleft in areas appeared atrophic with short clefts and coarse crests.

Conclusions​

Myopathic changes are common in Long COVID. sfEMG abnormality is less common but may correlate with clinical scores. sfEMG changes may be due to motor endplate pathology.

Significance​

These findings may indicate a muscle pathophysiology behind fatigue in Long COVID.

https://www.sciencedirect.com/science/article/pii/S1388245723000196?via=ihub

 

[pattismith]

Not myopathic, but autonomic changes in patients with long-COVID syndrome: a case series​

• Tommaso Bocci,
• Alessandro Bertini,
• Laura Campiglio,
• Stefano Botta,
• Giorgia Libelli,
• Matteo Guidetti &
• Alberto Priori

2023

Abstract​

Introduction​

Neurological sequelae following SARS-CoV-2 infection still represent a serious concern both for neurologists and neuroscientists. In our paper, we investigated pain, myalgia, and fatigue as symptoms in long-COVID patients with an electrophysiological approach, comprising the evaluation of sympathetic skin responses (SSRs) and quantitative electromyography (qEMG).

Materials and methods​

Twelve patients were enrolled (mean age, 47.7 ± 11.6 years), referred to our attention because of myalgia, pain, or muscle cramps, which persisted about 6 months after the diagnosis of SARS-CoV-2 infection. They underwent conventional electroneurography (ENG), needle electromyography (EMG), and SSRs; moreover, qEMG was performed by sampling at least 20 motor unit potentials (20–30 MUPs) during weak voluntary contraction in deltoid and tibialis anterior muscles. The mean duration, amplitude, and percentage of polyphasic potentials were assessed and compared with healthy and age-matched volunteers.

Results​

ENG did not disclose significant changes compared to healthy subjects; needle EMG did not reveal denervation activity. In addition, qEMG showed MUPs similar to those recorded in healthy volunteers in terms of polyphasia (deltoid: p = 0.24; TA: p = 0.35), MUP area (deltoid: p = 0.45; TA: p = 0.44), mean duration (deltoid: p = 0.06; TA: p = 0.45), and amplitude (deltoid: p = 0.27; TA: p = 0.63). SSRs were not recordable from lower limbs in seven patients (58%) and from the upper ones in three of them (25%).

Conclusion​

Our data suggest an involvement of the autonomic system, with a focus on cholinergic efferent sympathetic activity, without any evidence of myopathic changes.

https://link.springer.com/article/1...r&utm_medium=getftr&utm_campaign=getftr_pilot

 

[Osaca]

Thanks for sharing! Without reading into it, I would assume qEMG and sfEMG are quite a bit more advanced in comparison to the standard EMG which you can have done at your local hospital?

 

[Consul]

This reminded me of the article below on elevated atrogin-1 finding in mecfs.

Also I think research in mecfs have found increased utilization of proteins for fuel, maybe muscles are used as a source for those proteins.

http://followmeindenmark.blogspot.com/2020/08/atrogin-1-mrna-is-elevated-in-muscle.html?m=1

 

[JasonPerth]

Does this new finding support or challange this one?
https://x.com/resiapretorius/status/1696272269641764949?s=46&t=MKOhMke7DuglGcTS-Q6VQw

 

[SWAlexander]

No details yet on what kind of amyloid they found.
https://forums.phoenixrising.me/thr...-healthy-controls-after-i.90665/#post-2442121