| As I said in another comment, > These are politicized by certain patient advocacy groups and associated publishing circles but the evidence is considered pretty strong in the broader medical sphere. The “critiques” of the PACE study are mostly based around p-hacking the objectives until you get the results you want. PACE participants saw significantly fewer hospitalizations, lower mortality, and better reported questionnaire scores as a bonus. Because there is a lot of ire against recommending CBT among patient advocacy groups (including threatening to kill the authors and their families), some researchers have critiqued PACE because they have found some metrics in post-analysis that PACE did not improve (classic p-hacking). But that does not represent the broader view of the field. Described by other scientists: “[The critiques come from a] fairly small, but highly organized, very vocal and very damaging group of individuals who have, I would say, actually hijacked this agenda and distorted the debate so that it actually harms the overwhelming majority of patients.' > It shall not be dismissed as “proposed mechanism”. That is literally how the paper self described. I am linking you multiple RCTs demonstrating impact and you are linking speculative causes of a disease that do not yet meet Koch’s postulates. But even if a neurological mechanism holds up (not at all unlikely in my view), this is likely to not be the case for all populations currently diagnosed with long covid - but rather a subset. CBT will likely be helpful for both populations, given the evidence I have linked. My proof of my claim is that I have researched alternative treatments for long covid and CFS and none of them have these effect sizes :) If you have contrary evidence, that’s on you to prove, but fwiw I am not going to keep replying. And again, I’ve linked RCT evidence for the effectiveness of CBT in long covid, which I guess you have nothing to say about. |
Demonstrated effects of reactive microglia after COVID-19 include a reduction in oligodendrocytes and myelinated axons, highlighting disrupted myelin homeostasis.
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The UK Biobank study discussed above compared magnetic resonance imaging (MRI) data before and after SARS-CoV-2 infection in 401 individuals and 385 matched controls. MRI data obtained an average of 141 days following COVID-19 diagnosis revealed widespread structural abnormalities, including a small but significant global decrease in brain volume, changes throughout the olfactory system, and structural abnormalities in the limbic system, cerebellum, and major white matter tracts (fimbria and superior fronto-occipital fasciculus)
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Concordant findings in an MRI study of individuals with persistent cognitive impairment after COVID-19 found white matter hyperintensities correlating with verbal memory deficits
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Another imaging and neuropsychological assessment of 223 individuals who recovered from mainly mild to moderate SARS-CoV-2 infections and 223 matched healthy controls found that among the 11 MRI markers tested, significant differences between groups were found in global measures of mean diffusivity and extracellular free water, which were both elevated in the white matter of post-SARS-CoV-2 individuals
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And so on and so forth. Those are the first immediately obvious passages describing structural alterations to brain tissue in that one paper.
These are severe physiological issues. This is literal brain damage. This is a paper pointing to craters.