Abnormal brain diffusivity in participants with persistent neuropsychiatric symptoms after COVID-19, 2023, Liang et al.

Abnormal brain diffusivity in participants with persistent neuropsychiatric symptoms after COVID-19
Huajun Liang; Thomas Ernst; Kenichi Oishi; Meghann C. Ryan; Edward Herskovits; Eric Cunningham; Eleanor Wilson; Shyamasundaran Kottilil; Linda Chang

Objectives
We aimed to compare brain white matter integrity in participants with post-COVID-19 conditions (PCC) and healthy controls.

Methods
We compared cognitive performance (NIH Toolbox ® ), psychiatric symptoms and diffusion tensor imaging (DTI) metrics between 23 PCC participants and 24 controls. Fractional anisotropy (FA), axial (AD), radial (RD), and mean (MD) diffusivities were measured in 9 white matter tracts and 6 subcortical regions using MRICloud.

Results
Compared to controls, PCC had similar cognitive performance, but greater psychiatric symptoms and perceived stress, as well as higher FA and lower diffusivities in multiple white matter tracts (ANCOVA-p-values≤0.001–0.048). Amongst women, PCC had higher left amygdala-MD than controls (sex-by-PCC p=0.006). Regardless of COVID-19 history, higher sagittal strata-FA predicted greater fatigue (r=0.48-0.52, p<0.001) in all participants, and higher left amygdala-MD predicted greater fatigue (r=0.61, p<0.001) and anxiety (r=0.69, p<0.001) in women, and higher perceived stress (r=0.45, p=0.002) for all participants.

Conclusions
Microstructural abnormalities are evident in PCC participants averaged six months after COVID-19. The restricted diffusivity (with reduced MD) and higher FA suggest enhanced myelination or increased magnetic susceptibility from iron deposition, as seen in stress conditions. The higher amygdala-MD in female PCC suggests persistent neuroinflammation, which might contribute to their fatigue, anxiety, and perceived stress.

Link | PDF (NeuroImmune Pharmacology and Therapeutics)

 

See threads tagged with myelin and in particular —

Myelin lipid metabolism and its role in myelination and myelin maintenance (2022)

These findings may relate to the observations of increased brainstem volume and white matter variation in —

Brainstem volume changes in myalgic encephalomyelitis/chronic fatigue syndrome and long COVID patients (2023)
Anti-Correlated Myelin-Sensitive MRI Levels in Humans Consistent with a Subcortical to Sensorimotor Regulatory Process (2022)

 

Then you tested it wrong. Cognitive impairment is one of the most reported issues, and one of the most disabling. This is not credible.

And clearly, badly want to attribute this to "stress", which is always poorly assessed and without any depth. I don't even understand what chronic stress as a condition could mean. It's a factor, not a condition in itself, and being disabled without support is always stressful, especially if it's defined through the most common symptoms of illness.

It's frankly looking more and more as if the obsessive need to prove psychogenic stuff is taking up most of the motivation overall. Trying very hard to show a specific direction of causality, and only the one.

This isn't good science, it is too biased. Even when they find things, they scramble to attribute them to the traditional stuff. Instead of solving problems, they're trying to reassess past failures and give them all new excuses, that happen to be the exact same old.

 

Yes I did wonder whether I should write a caveat to ignore the suggested mechanisms, esp with regard to stress. The classification of all these symptoms as neuropsychiatric is of course unevidenced.

I don't know why the included criteria included memory complaints, brain fog and yet the results showed —

Anyhow the key thing about this paper as I see it is the evidence for alteration in the microstructure of white matter. They give three possible explanations, with an increase in myelination suggested to fit the best both mechanistically and in relation to the imaging evaluation. This is interesting given the observations of increased brainstem volume in ME. As I indicated in my post #5, I think this points to the possibility of systemic alterations in metabolism (esp lipid metabolism) leading on to changes in myelin, that then might reflect in symptoms. Also interesting that neuroinflammation seemed not to be evidenced in this study.