Abstract Following infection from SARS-CoV-2, a substantial minority of people develop lingering after-effects known as ‘long COVID’. Fatigue is a common complaint with substantial impact on daily life, but the neural mechanisms behind post-COVID fatigue remain unclear. We recruited 37 volunteers with self-reported fatigue after a mild COVID infection and carried out a battery of behavioural and neurophysiological tests assessing the central, peripheral and autonomic nervous systems. In comparison to age and sex matched volunteers without fatigue (n = 52), we show underactivity in specific cortical circuits, dysregulation of autonomic function, and myopathic change in skeletal muscle. Cluster analysis revealed no sub-groupings, suggesting post-COVID fatigue is a single entity with individual variation, rather than a small number of distinct syndromes. Based on our analysis we were also able to exclude dysregulation in sensory feedback circuits and descending neuromodulatory control. These abnormalities on objective tests may aid in the development of novel approaches for disease monitoring. Open access, https://academic.oup.com/braincomms/advance-article/doi/10.1093/braincomms/fcad122/7115845
Interesting paper, I've read about half of it. The authors are from Newcastle University, and aim to test if any of a slew of neurological tests can indicate which of 5 potential hypothesized pathologies of fatigue would apply to Long Covid patients (6-26 weeks after infection, average fatigue impact score of around 80/160).
Yes, interesting. Lots of overlap, but still some significant differences. I don't have the background to evaluate this, but I liked the systematic approach to testing, and the evaluation against the hypotheses. Hypothesis 1 - a problem with brain's control of motor neurons - some evidence to support this There was one measure supporting this, but a number of other measures not supporting the hypothesis. There was a trend to longer visual reaction times which would support this, but the P-values weren't significant after adjustment for multiple comparison. Hypothesis 2 - a problem with sensory feedback processing - no evidence to support this From the reference Kuppuswamy: Hypothesis 3 - a problem with the function of muscles - evidence to support this On the basis of increased peripheral fatigue during a prolonged maximal contraction, the authors concluded that this could indicate metabolic changes in muscle fibres after prolonged activity, leading to reduced force output. That leads to a stronger voluntary drive and a higher perceived effort. The authors didn't think that the connections between the motoneurons to the muscle fibres was a problem. Hypothesis 4 - a problem with the motorneuron responses - no evidence to support this Hypothesis 5 - autonomic dysregulation - some evidence to support this The increased heart rate finding was consistent with autonomic dysregulation. There were also some trends to a number of other measures supporting autonomic dysregulation. They note that these findings, including temperature, and also the reduced oxygen saturations, could be related to long-lasting impacts of the acute infection on lung function and immune activation. I had the impression that any temperature difference in ME/CFS tended to lower temperatures, not higher. On the oxygen saturations:
Followed up in Recovery of neurophysiological measures in post-COVID fatigue: a 12-month longitudinal follow-up study (2024, Nature Scientific Reports)
