Higher limbic and basal ganglia volumes in surviving COVID-negative patients and the relations to fatigue, 2022, Hafiz, Natelson et al

Andy

Retired committee member
Abstract

Background
Among systemic abnormalities caused by the novel coronavirus, little is known about the critical attack on the central nervous system (CNS). Few studies have shown cerebrovascular pathologies that indicate CNS involvement in acute patients. However, replication studies are necessary to verify if these effects persist in COVID-19 survivors more conclusively. Furthermore, recent studies indicate fatigue is highly prevalent among ‘long-COVID’ patients. How morphometry in each group relate to work-related fatigue need to be investigated.

Method
COVID survivors were MRI scanned two weeks after hospital discharge. We hypothesized, these survivors will demonstrate altered gray matter volume (GMV) and experience higher fatigue levels when compared to healthy controls, leading to stronger correlation of GMV with fatigue. Voxel-based morphometry was performed on T1-weighted MRI images between 46 survivors and 30 controls. Unpaired two-sample t-test and multiple linear regression were performed to observe group differences and correlation of fatigue with GMV.

Results
The COVID group experienced significantly higher fatigue levels and GMV of this group was significantly higher within the Limbic System and Basal Ganglia when compared to healthy controls. Moreover, while a significant positive correlation was observed across the whole group between GMV and self-reported fatigue, COVID subjects showed stronger effects within the Posterior Cingulate, Precuneus and Superior Parietal Lobule.

Conclusion
Brain regions with GMV alterations in our analysis align with both single case acute patient reports and current group level neuroimaging findings. We also newly report a stronger positive correlation of GMV with fatigue among COVID survivors within brain regions associated with fatigue, indicating a link between structural abnormality and brain function in this cohort.

Open access, https://www.sciencedirect.com/science/article/pii/S2666956022000198
 
Although that's nice and everything, it can't explain the relapsing-remitting pattern or PEM. So it can't have a significant impact on fatigue, as fatigue could not wildly change without matching changes in those regions if it's a significant cause.

It certainly doesn't explain how some can have severe fatigue during the acute phase, feel better for a short while, get a bit worse, get a bit better, then massively worse. Or how some have seen improvements from vaccination or medication. Or worsened. Many patients had severe increase in symptoms following vaccination. Obviously it didn't cause those brain regions to shrink rapidly enough to explain the symptoms.

The typical model of medical research where they try to pick apart one part of the whole and isolate it cannot work here. It fails at basic coherency, at respecting what's actually happening to the patients. The whole thing where symptoms can be detached from their context is simply absurd, and I'm starting to think this may be one of the biggest reasons for the stagnation of medicine. Decades of trying to smash square things into round holes doesn't make them fit any better.
 
It looks like this was done only 2 weeks after hospital discharge, so not necessarily any relevance to longer term post Covid symptoms. It just shows a correlation between fatigue and the volume of the parts of the brain associated with fatigue.
 
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