How research directions and patient experiences connect to the terms ME, CFS and future names

[Hoopoe]

The hypothalamic dysfunction makes sense. In my case symptoms were initially interpreted as indicating a pituitary, adrenal or thyroid disorder. There were some abnormalities, but not consistent with any specific diagnosis in this category. At the time the symptoms and abnormalities included unrefreshing sleep, mildly low blood pressure, initial orthostatic hypotension, episodes of mild hypoglycemia, fatigue, low stress tolerance, abnormal diurnal cortisol curve, a tendency to crash after trying to resume normal activity levels and responsibilities, poor thermoregulation. I also experienced symptoms that were more typical of a mood disorder like social withdrawal, depressive mood, and outbursts of anger but I view these more as reaction of an adolescent to the adverse situation represented by the illness itself and the experience of not being understood.

Also I have an empty sella which may be relevant. During an ACTH stimulation test I had a panic attack which indicates an abnormal reactivity of some kind. I read this can be either hypothalamic in origin or due to increased receptor sensitivity.

 

[Tom Hill]

Which might bring in age-dependent instability of hypothalamic co-ordination

But if this were the cause of why people tend to get me/cfs as adolescents or circa 40 (or, in another interpretation, why rates drop off after 40ish, rather than peak strictly speaking) then we’d see a lot more me/cfs onset from a much wider range of viruses, wouldn’t we? As they would all set up the hypothalamic reset challenge, I’d imagine. A specific set of neurotropic viruses seem in a class of their own in me/cfs onset.

 

[Mij]

It always just makes me think of the French énervé (annoyed) and ça m'énerve (that p****s me off, that drives me mad).

Exactly what I interpreted until I looked up enervate.

Comment calmer une sensation de malaise? oof

 

[Jonathan Edwards]

The members here who seem confident that studying the immune system further is a waste of resources

I think, to be fair, people are against studying aspects of immune responses that already look very likely to be blind alleys.

 

[V.R.T.]

I think, to be fair, people are against studying aspects of immune responses that already look very likely to be blind alleys.

I'm against that too! Although perhaps we might not all agree on what the blind alleys are likely to be...

 

[Jonathan Edwards]

we’d see a lot more me/cfs onset from a much wider range of viruses, wouldn’t we? As they would all set up the hypothalamic reset challenge, I’d imagine.

Maybe we do. Maybe the focus on EBV is heavily biased by how dramatic that can be and the fact that there is an antibody test (which doesn't discriminate very well between recent and old infection). It does seem likely that EBV is particularly prone to trigger ME/CFS but that might simply be because it produces very high and repeated fevers. It also leads to major CD8 cell recruitment directed at self B cells. The hypothalamus may well be susceptible to signals from those events. But it may also be susceptible to concussion, or other things.

 

[Tom Hill]

Maybe the focus on EBV is heavily biased by how dramatic that can be and the fact that there is an antibody test (which doesn't discriminate very well between recent and old infection). It does seem likely that EBV is particularly prone to trigger ME/CFS but that might simply be because it produces very high and repeated fevers.

That’s very interesting that EBV’s importance may be a mirage. But that’s a really big and powerful mirage given, for adolescents, the phrase “she/he’s not in school due to glandular fever” is essentially synonymous with “due to me/cfs/PVFS”.

And then there’s the big surge that’s come with COVID. Don’t think we’ve seen me/CFs surges during unusually bad flu seasons, for example.

I got dengue fever on field work once, and it had an unusually high fever sustained for an unusually long time. I could just be a random piece of data, of course, but it didn’t bring on me/cfs in my case, and I don’t think it’s been noted anywhere as a known me/cfs onset disease. Both my confirmed covid infections [the first of which brought on me/cfs] didn’t involve high fever.

 

[Mij]

Both my confirmed covid infections didn’t involve high fever

Incase you're interested, we have a thread on Lack of Fever during infections

I never had a fever during sudden-viral onset ME or Covid. During sudden-onset a viral infection attacked my thyroid, fever is a big symptom, but I didn't have fever at all.