"Physicians like disease & injury to be visible, if they are going to accept it as real."

I'm going to start w/ a focus on #MECFS, and then round out this tweet-thread w/ a segway onto why all this matters for #longcovid, too. This chronology is poetically fitting, at any rate.
We know by now that #MECFS brains are generally replete w/ neuroinflammation. PET & MRSt scans demonstrate this readily and consistently.
We know by now that metabolites, like lactate, choline-containing compounds, myo-inositol, & N-acetylaspartate, are considerably altered in #MECFS brains, and this is readily demonstrated via MRS scanning.
We've known for decades now that #MECFS brains have ubiquitous blood-flow abnormalities, marked by hypoperfusion, w/ the brainstem (which controls autonomic functions) standing out according to SPECT scanning.
So we have PET, MRS, MRSt, and SPECT scans that all have the potential to identify differences between a MECFS brain and healthy controls.

"Physicians like disease & injury to be visible, if they are going to accept it as real."
But for the most part, the medical community tends to rely on CT/MRI scans, w/ which "diffuse cellular and microvascular injuries are [generally] invisible."
Indeed, patients themselves tend to request CT/MRI's all-the-same, but if we don't perform the most appropriate scan, we're not going to get results that a medical professional can "see to believe."
MECFS brains are defined by neuroinflammation, as well as metabolite & blood-flow irregularities (hypoperfusion).

The research overwhelmingly delineates that we should probably expect the same for #COVID19/#longcovid brains, as well.

Shit, 86-100% of deceased #COVID19 brains demonstrate immune profiles that denote damage/injury has occurred.

Plenty of #longhaulers have had CT/MRI's done w/ nothing of substance to note, despite the slew of neurological syndromes the grand majority exhibit. It's the same song & dance, and what MECFS dealt with for decades, #COVID19 longhaulers are dealing with now.
The medical community can't drag its feet anymore. The longhauler community will, naturally, push & pull frantically in all sorts of often redundant directions. But the medical community has no excuse. You're capable of understanding what's going on, and w/ efficiency.
SPECT, PET, MRSt. The technology has improved. Let's now make the technology more pervasively distributed & readily accessible, and let's get more medical professionals informed on how/when to apply & utilize them.

I speak for #pwME when I say that the wait should be over.

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More from @FizeekBio

30 Apr
I develop fixations in my studies. I develop fixations on elements that present promise in connecting dots. It's all one big puzzle, and my goal is to make the pieces fit. I can't do it without developing these fixations.

#SARSCoV2, microclots, infarcts, multi-organ damage.
#SARSCoV2 inhibits Type-1 interferon (IFN). This is its evolutionary advantage over its predecessor SARSCoV, & likely the reason behind the asymptomatic phenomenon, since IFN ➡️ immune activation, inflammation, fever ➡️ symptoms.

This is what makes #COVID19 special. Image
We also know that IFN is critical in facilitating a switch from innate immunity (nonspecific defenses like neutrophil NETosis & platelet-induced coagulation) to adaptive immunity (highly specific defenses involving T/B cells & antibody production). Image
Read 8 tweets
15 Oct 20
The immune-response and #COVID19. The "Wack-a-Mole" theory.

This is going to be heavy, and technical at points. But it's important that I regurgitate my thoughts. This is my Eureka moment. #SARS_CoV_2
#COVID degrades the epithelial cells of the lungs, and begins infiltrating therein via the epithelial cells of the underlying vasculature. Image
The immune system reacts by tipping the balance towards clotting (releasing factors that make the blood more “sticky” and conducive to clotting), in effort to stall the intruders right in their point of entry before entering the wider circulatory system.
Read 16 tweets

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