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@ARTICLE{Dadsena:281778,
author = {Dadsena, Ravi and Wetz, Sophie and Hofmann, Anna and Costa,
Ana Sofia and Romanzetti, Sandro and Lischewski, Stella
Andrea and Krockauer, Christina and Balloff, Carolin and
Binkofski, Ferdinand and Schulz, Jörg B and Reetz, Kathrin
and Walders, Julia},
title = {{E}vidence of clinical and brain recovery in
post-{COVID}-19 condition: a three-year follow-up study.},
journal = {Brain communications},
volume = {7},
number = {5},
issn = {2632-1297},
address = {[Oxford]},
publisher = {Oxford University Press},
reportid = {DZNE-2025-01173},
pages = {fcaf366},
year = {2025},
abstract = {Fatigue and cognitive dysfunction linked to persistent
brain changes have been reported for up to two years after
COVID-19. In this study, we followed the clinical,
neuroimaging and fluid biomarker trajectories over three
years post SARS-CoV-2 infection to evaluate potential signs
and underlying factors of brain recovery. We conducted a
monocentric, longitudinal study using resting-state
functional and structural T1-weighted magnetic resonance
imaging data from 51 patients with post-COVID-19 condition
(mean age 50 years, 33 female) collected at a mean time of
6, 23 and 38 months after COVID-19 infection. The trajectory
of brain changes was compared to 23 age- and sex-matched
healthy controls (mean age 37 years, 13 female) with similar
time intervals between brain scans and analysed in relation
to clinical, neuropsychological and fluid biomarkers
including interleukins and neurodestruction markers at all
timepoints. In addition, hand grip strength to evaluate
muscular fatigue was assessed at the final follow-up visit.
Self-reported fatigue improved over time but was still
moderate on average three years after COVID-19 infection,
while measures of hand grip strength and cognitive
performance were largely unaffected. We found a significant
increase of both lateral ventricles $(∼8\%)$ and the third
$(∼6\%)$ ventricle accompanied by a structural volume
reduction in adjacent areas including the thalamus,
pallidum, caudate nucleus and putamen. An increased neuronal
activation pattern was widespread and pronounced in these
areas. The brainstem no longer exhibited volume loss as
reported in our pervious study, but enhanced functional
connectivity. Laboratory markers including interleukins and
neuronal injury markers remained within the normal reference
ranges across all study timepoints. Our study revealed an
overall slow but evident clinical improvement, including
improved fatigue, regular muscular strength and recovery as
well as normal cognitive function without signs of systemic
inflammation three years after COVID-19. Clinical
improvement is reflected by a pattern of brain recovery
along periventricular regions. This pattern is characterized
by structural stabilization and increased connectivity
starting in the brainstem as well as efficient neuronal
recruitment and increased activation in the basal ganglia,
with no evidence of neuronal injury. These results highlight
the positive long-term recovery trajectory in post-COVID
patients.},
keywords = {ALFF (Other) / CNS (Other) / MRI (Other) / fatigue (Other)
/ long COVID (Other)},
cin = {AG Jucker},
ddc = {610},
cid = {I:(DE-2719)1210001},
pnm = {352 - Disease Mechanisms (POF4-352)},
pid = {G:(DE-HGF)POF4-352},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41079753},
pmc = {pmc:PMC12508649},
doi = {10.1093/braincomms/fcaf366},
url = {https://pub.dzne.de/record/281778},
}