What can the science on the impact of acute infections on cognition tell us about ME/CFS?

[ScoutB]

Perhaps a bit off-topic, but was wondering if ME/CFS is like sickness behavior, why we don't see more loss of appetite.

For what it's worth, I definitely have loss of appetite (I say, as I force myself to eat a bowl of perfectly good soup). I wonder if it could be more common than we know because it's not as acutely debilitating as other symptoms?

So a possible answer is that during normal infection multiple pathways normally occur in tandem that affect the brain, but only particular ones are active in ME/CFS.

This would definitely validate what it feels like is going on for me. Also, there's so much variability even in one person with how they react to different bugs (sometimes you get a fever, sometimes not, sometimes your muscles ache, other times you're just utterly physically exhausted). I figured there must be a lot of flexibility around which particular pathways get triggered when your body decides it's time to feel sick.

 

[AliceLily]

Perhaps a bit off-topic, but was wondering if ME/CFS is like sickness behavior, why we don't see more loss of appetite.

I experienced a lot of loss of appetite in my severer years. I felt sick and poisoned and I remember describing somewhere where it felt like three different types of nausea that I would experience. Possibly on top of each other at times. I lost a stone in weight at my very severe onset and whenever I did put weight back on I would get a severe PEM and lose it again. My ME did not like me carrying any extra weight in the severer years.

 

[Jonathan Edwards]

So a possible answer is that during normal infection multiple pathways normally occur in tandem that affect the brain, but only particular ones are active in ME/CFS.

Yes, I put my money on this.
I think 'sickness behaviour' is one of those ragbag terms that can be useful but was never going to cover just one process.

A similar situation applies to inflammation where you have shifts in water and protein permeability plus cell emigration. Different mediators affect the two processes differently. Histamine largely changes permeability. TNF alters cell migation by upregulating adhesion molecules. As a result we can sometimes distinguish purely transudative inflammation from exudative inflammation. In lupus both occur, with different clinical consequences. Prostanoids also link in to the third aspect of pain, which in RA can be severe or largely absent, independent of cytokine mediated damage. And so on.

 

[hotblack]

Like @Peter T this is a bit of an extreme example but the real decline in my health occurred after a kidney infection which went bad. I’d been sent home with antibiotics but woke up very early one morning with an intense feeling of something being very very wrong. I became increasingly weak, unable to walk or think straight, very confused, almost dissociative. It was unlike anything I’ve experienced before even with fever.

I was taken by family to an out of hours dr at the hospital who immediately admitted me with suspected sepsis where I don’t think it’s an exaggeration to say they saved my life. But despite ups and downs I never fully recovered.

I didn’t understand people talking of ‘flu like’ symptoms because that wasn’t what me/cfs was like for me. It was a generally much lower ability to do things but particularly characterised by these more extreme episodes similar to those I experienced with that acute infection. But which occurred after activity.

But as it has gone on, during my better periods I do know what people mean. There is something more like a usual illness. Where I can just sort of curl up and rest. But I also still have those periods when my body really does feel like it’s in ‘wtf’ mode and something quite different is happening.

The idea of different pathways, or a subset of them being relevant makes sense. Maybe exactly which helps define severity and symptom profiles?

 

[hotblack]

I also experience loss of appetite and lost a lot of weight early on, as others who are have mentioned. I’ve learnt to force myself to eat even if it’s a struggle (either because of loss of appetite, feeling nauseous, food being off putting or just physically hard to eat) because letting those processes shut down is not a good path.

 

[AliceLily]

For what it's worth, I definitely have loss of appetite (I say, as I force myself to eat a bowl of perfectly good soup). I wonder if it could be more common than we know because it's not as acutely debilitating as other symptoms?

I also experience loss of appetite and lost a lot of weight early on, as others who are have mentioned. I’ve learnt to force myself to eat even if it’s a struggle (either because of loss of appetite, feeling nauseous, food being off putting or just physically hard to eat) because letting those processes shut down is not a good path.

I had to force myself to eat as well. I did have some windows of opportunity where I suddenly had an appetite, usually late in the evening. Not often due to severe PEM but when I did I would eat as much good food as I could when this happened.

I should add that this was in my severer years.

 

[hotblack]

The idea of different pathways, or a subset of them being relevant makes sense. Maybe exactly which helps define severity and symptom profiles?

Expanding on this a bit, the two questions this raises for me

- Could it be the case that whatever triggering event, or even subsequent triggers, activate particular pathways which characterise the variations in our illness? (This may also be affected by underlying genetic predisposition)

- Could here be something whereby different pathways are active which causes the symptoms and if enough of them are you get this extra/extreme response which occurs less frequently? A sort of cumulative threshold which explains some of those things we see in very severe ME/CFS?

 

[duncan]

Perhaps a bit off-topic, but was wondering if ME/CFS is like sickness behavior, why we don't see more loss of appetite.

Sickness behavior implies an observer. It involves a third party perspective. Little wonder it was coined by a veterinarian because his patients couldn't directly communicate how they felt. He had to infer.

And by virtue of the word "behavior", thanks to the BPS cult, sickness behavior is loaded with risk to the long term sick. It helps delegitamize patient reports, potentially foisting them on to some other form of authority.

Being sick is pure subjective experience; experience that may or may not be supported through objective tests.

What are the implications to cognitive impairment? If constructs such as sickness behavior for humans really take hold, with the absence of relevant accurate cognitive testing, patients with cognitive deficits may get kicked to the curb. They already are.

 

[ScoutB]

And by virtue of the word "behavior", thanks to the BPS cult, sickness behavior is loaded with risk to the long term sick. It helps delegitamize patient reports, potentially foisting them on to some other form of authority.

Yes I get your point about it being from an observer’s point of view and I could see BPS types trying to use the term to psychologize patient’s responses to being ill. It’d be nice if we had a better name for this thing.

(The fact that it comes out of studies of animals really should suggest the opposite, that these are normal, unavoidable features of being an ill animal, but alas.)

It feels useful to be able to talk about this collection of symptoms/signs. I’m hoping that once the biology here is better understood it’ll make it more obvious to medicine that the BPS ideas are completely wrong.