Thread by @jenbrea

PEM (post-exertional malaise) may be “exertion-triggered tissue hypoxia.” Yes, I have been saying this! This is rad. Can’t wait to check out the paper… #MECFS #longCOVID

https://twitter.com/Be_Kinderr/status/1430206909387362306

If true, this is probably why Chiari, CCI/AAI, tethered cord, cerebral vascular stenosis, MALS, and Nutcracker Syndrome, et al. can cause PEM in a subset of #MECFS patients: they can all cause tissue hypoxia, producing similar symptoms to other causes of tissue hypoxia.

(*and #longCOVID)

It’s worth mentioning that a longtime patient, Maryann Spurgin, first pointed me to the work on blood flow in #MECFS, although I did not understand its relationship to PEM at the time. (I don’t know her view on structural pathologies.) We’ve known this to some degree for decades.

It’s also worth mentioning that when we say “tissue hypoxia” in #MECFS, we are probably talking primarily about nerve tissue: brain, spinal cord, and peripheral nerves. This is why our experience of the illness feels systemic…because our nervous system is everywhere!

I say that in part because of the existing evidence of cerebral hypoperfusion (poor/abnormal brain blood flow), about which there have been a number of studies: me-pedia.org/wiki/Brain#Blo…

The flip side of poor brain blood flow is intracranial hypertension, which has been suggested to be present in a significant subset of patients: me-pedia.org/wiki/Intracran…

Why is this the flip side? The cranium is a fixed space, and in most cases outside of acute trauma, if you have elevated pressure in the brain, it’s going to be from either excess CSF or excess blood (e.g., due to poor drainage).

In fact, a 2011 study found “impaired cerebral vascular auto regulation” in #MECFS patients [1] …iencejournals.onlinelibrary.wiley.com/doi/full/10.10…, which might account for the similarities between ME and TBI [2] ncbi.nlm.nih.gov/pmc/articles/P…

All this has been right out there, in the open, in the history of this diagnosis but we’ve gotten so far away from clinical medicine and neurology—primarily because these are the systems that have most abused and neglected us—that a lot has been misunderstood or forgotten.

Don’t get me wrong, molecular biology is important, but if we aren’t connecting the very small to the very large (gross anatomy, epidemiology), we run the risk of wading in findings that are secondary or tertiary to the actual problem.

Every paper that looks at a molecular mechanism for impaired energy production in #MECFS MUST contend with the finding that ME patients have impaired blood flow and explain how their molecular mechanism has explanatory power above and beyond what we already know hypoxia can do.