Structural brain changes in patients with post-COVID fatigue: a prospective observational study, 2023, Heine, Scheibenbogen et al

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SNT Gatchaman

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Structural brain changes in patients with post-COVID fatigue: a prospective observational study
Josephine Heine, Katia Schwichtenberg, Tim J. Hartung, Sophia Rekers, Claudia Chien, Fabian Boesl, Rebekka Rust, Christian Hohenfeld, Julia Bungenberg, Ana S. Costa, Carmen Scheibenbogen, Judith Bellmann-Strobl, Friedemann Paul, Christiana Franke, Kathrin Reetz, Carsten Finke

Background
Post-COVID syndrome is a severe long-term complication of COVID-19. Although fatigue and cognitive complaints are the most prominent symptoms, it is unclear whether they have structural correlates in the brain. We therefore explored the clinical characteristics of post-COVID fatigue, describe associated structural imaging changes, and determine what influences fatigue severity.

Methods
We prospectively recruited 50 patients from neurological post-COVID outpatient clinics (age 18–69 years, 39f/8m) and matched non-COVID healthy controls between April 15 and December 31, 2021. Assessments included diffusion and volumetric MR imaging, neuropsychiatric, and cognitive testing. At 7.5 months (median, IQR 6.5–9.2) after the acute SARS-CoV-2 infection, moderate or severe fatigue was identified in 47/50 patients with post-COVID syndrome who were included in the analyses. As a clinical control group, we included 47 matched multiple sclerosis patients with fatigue.

Findings
Our diffusion imaging analyses revealed aberrant fractional anisotropy of the thalamus. Diffusion markers correlated with fatigue severity, such as physical fatigue, fatigue-related impairment in everyday life (Bell score) and daytime sleepiness. Moreover, we observed shape deformations and decreased volumes of the left thalamus, putamen, and pallidum. These overlapped with the more extensive subcortical changes in MS and were associated with impaired short-term memory. While fatigue severity was not related to COVID-19 disease courses (6/47 hospitalised, 2/47 with ICU treatment), post-acute sleep quality and depressiveness emerged as associated factors and were accompanied by increased levels of anxiety and daytime sleepiness.

Interpretation
Characteristic structural imaging changes of the thalamus and basal ganglia underlie the persistent fatigue experienced by patients with post-COVID syndrome. Evidence for pathological changes to these subcortical motor and cognitive hubs provides a key to the understanding of post-COVID fatigue and related neuropsychiatric complications.

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So it would also be really good to have some matched controls with pwME using IOM criteria.

Subcortical regions, no surprise there, but with all this research coming out on the effects of the virus on the brain...and major implications for the health/care/disability agencies/economies and the person with LC.
 
Ugh. Here they go again with "cause" of fatigue in the news article. It correlates, we don't know if it's causative at all. In fact there is no need to bring brain atrophy into this, the crippling exhaustion during illness, say a flu, obviously does not cause rapid brain atrophy.

Medicine really has to stop thinking of the brain as this master conductor that knows and runs everything. It isn't at all. We are a whole freaking organism, damnit. It's also not a smart top-down process, it's an evolutionary kludge that works just well enough for our species to reproduce. It doesn't have to make sense, in fact nothing in biology does.

Interesting result for sure but this obsession with clicks and eyeballs has to stop, medicine really has to rein in speculative claims like this. It's almost as click-baity as Internet influencers at times.

Maybe brain atrophy will be taken seriously. But it's not established that it's the cause of fatigue. In fact it literally doesn't make sense since it fluctuates enormously, whereas the brain atrophy does not, cannot.
 
hibiscuswahine said:
So it would also be really good to have some matched controls with pwME using IOM criteria.
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29% of participants (12/41) met IOM ME/CFS criteria

So even if a small sample, would it be worthwhile to do a sub-group analysis?

Also I wonder whether it's possible to compare the scans with the recent findings of changes in brainstem volumes -- discussed on theforum here.


(That's what I wonder anyway: there must be so many samples of brain scans of pwME done by diverse study teams, each I assume with adequate control groups -- if they find structural differences, why don't the teams exchange their findings, share the scans? -- Genuine question.)
 
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Fatigue is characterised by an overwhelming experience of weakness, exhaustion, and decreased capacity for physical or mental work which is disproportional to recent activity.6, 7, 8 Fatigue is a complex phenomenon at the interplay of central regulation (i.e., homeostasis) and psychological factors like mood and motivation.6,7,9 In PCS, the experience of fatigue is frequently accompanied by muscle fatigue and fatiguability, which can be assessed by hand grip strength and correlates with biomarkers for inflammation and hypoperfusion.10 A subset of patients with PCS fulfil the diagnostic criteria for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a complex disease in which fatigue is accompanied by exertional intolerance and post-exertional malaise. Environmental stressors may additionally contribute to fatigue through changes in the neuroendocrine stress response, altering the hypothalamic-pituitary-adrenal and norepinephrine systems
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Central fatigue impacts psychosocial and cognitive functions and is often perceived as most distressing by patients.7 In fact, fatigue is one of the main contributors to post-COVID disease burden.11
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[Edited: My bolding]
 
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