Science News: Myopathy as a Cause of Long COVID Fatigue: Evidence From Quantitative and Single Fiber EMG and Muscle Histopathology
Published October 13, 2023
Science News
Submitted by: Eman Tawfik, MD
Edited by: Pritikanta Paul, MD
Edited by: Pritikanta Paul, MD
Citation: Agergaard J, Yamin Ali Khan B, Engell-Sørensen T, et al. Myopathy as a cause of Long COVID fatigue: Evidence from quantitative and single fiber EMG and muscle histopathology. Clin Neurophysiol. 2023;148:65-75. doi:10.1016/j.clinph.2023.01.010
Summary: Long COVID is a long-term disabling sequalae of COVID-19 infection in hospitalized patients as well as in patients with mild symptoms. A common presenting symptom is physical fatigue. The author of this study previously reported myopathic changes in quantitative EMG (qEMG) and pathological changes in muscle biopsies of a small group of long COVID patients with fatigue. In this study, the authors investigated the clinical and electrodiagnostic features in a larger cohort of long COVID patients to explore whether myopathy and neuromuscular transmission failure are common causes of post-COVID fatigue.
The patients were recruited from a post-COVID clinic in Denmark from December 2020 to March 2022. Patients with impaired daily function and physical/muscular fatigue, myalgia, or reduced muscle force who were referred for qEMG were included. Critically ill patients and patients with known neurological disease were excluded.
All patients underwent motor nerve conduction studies (NCSs) of the tibial and peroneal nerves and sensory NCS of the peroneal and sural nerves, repetitive nerve stimulation (RNS) of the median and spinal accessory nerves, qEMG of the biceps, vastus medialis, and tibialis anterior muscles using concentric needle, and single fiber EMG (sfEMG) of the tibialis anterior and later extensor digitorum communis muscles. Additionally, muscle biopsy from the biceps brachii with examination using light and electron microscopy was performed.
A total of 84 patients meeting the study's inclusion criteria were enrolled. None of these patients exhibited abnormal nerve conduction studies (NCSs) or repetitive nerve stimulation (RNS) results. In 52% of the patients, there was a reduction in the mean duration of motor unit potential (MUP) in at least one muscle. Additionally, an increase in mean jitter was noted in 17% of the patients, specifically in the tibialis anterior muscle, and in 25% of the patients in the extensor digitorum communis muscles. The heightened jitter was observed in patients with or without myopathic quantitative electromyography (qEMG) findings. Furthermore, muscle biopsies revealed the presence of damaged terminal nerves and motor endplates, accompanied by an abundance of basal lamina material. The post-synaptic cleft displayed atrophy with short clefts and coarse crests.
The authors suggested that sfEMG changes may be due to motor endplate pathology. The myopathic changes being observed in > 50% of the patients could be the underlying cause of fatigue in long COVID patients.
Comments: The article provides valuable insight into the electrophysiological abnormalities in long COVID patients with physical fatigue. The myopathic changes in >50% patients with long COVID fatigue symptoms are of particular interest. It would be interesting to perform muscle ultrasound examinations and correlate the structural changes observed with ultrasound and the electrophysiological and muscle biopsy findings.