What do we mean by a diagnosis like ME/CFS?

What Trish has written is also largely how I have understood things to be.

I however wonder about this part a bit and what it is supposed to me. My understanding is that ME/CFS always involves disabling fatigue (very different from tiredness or fatigue occuring commonly in life), PEM (which is largely defined via the other core symptoms that are present as is described as their worsening after exertion in addition to possible new symptoms, such as sore troat, flu-like feelings of malaise, myalgia etc and at last regularly occurs delayed and does not follow usual time patterns of "getting better" seen elsewhere, and is not resolved by sleep) and some other core symptoms which however might vary to some degree (cognitive issues, OI, sleep dysfunction, etc) and that current syndrome definitions are focused on delayed PEM as this is supposedly a meaningful differentiator between what is seen in other illnesses and/or healthy people. Psychiatry has chosen to focus on any kind of fatigue to keep things vague and muddying the waters whilst expanding the reach.

What I don't quite understand is what rapid and disabling fatiguability is supposed to mean in this context as central part of the picture?

 

In a way yes, but there is a crucial extra, hidden, component to the syndrome concept. A clinical pattern is only a syndrome if we have at least a hunch that there is some common component to the causation that is medically relevant. It does not need to be the original cause, just some common part of the pathways.

The point being that you could pick out all the people who keep being off sick on Thursdays to go to hospital as distinctive, or all the people whose gout is in the ring finger as distinctive but these are not syndromes because the common causality is trivial or irrelevant (the receptionist first booked them on to a Thursday clinic because it was the next slot available).

There have been many putative syndromes that are probably not syndromes at all. PoTS is said to be a syndrome but I think it very likely that even if one can produce 'diagnostic criteria' for a clearly definable group of people it is not a real syndrome because it does not pick out any particular causal path with good specificity and sensitivity. Fibromyalgia was at one time seen as a syndrome of specific tender points until it was discovered that there are no specific tender points.

 

@Jonathan Edwards, does this phenomenon tend to occur in rheumatological or other diseases? I don't mean relief when a flare settles down, I mean improvements that can't really be explained by treatment or management.

Struggling to get my foggy brain around whether this is a meaningless way of looking at it because it doesn't compare like with like. There's no tissue damage in ME/CFS that could potentially heal, and conditions like psoriasis might remit or go away but they don't improve.

 

There are unexpected and rapid remissions in other conditions for which we do not have full explanations but at leat we tend to have some understanding of what may be occurring in the relevant time frame. It is complicated. I do not know a lot about the time course of psoriasis itself but clearly it can be unpredictable.

 

Thank you. Still trying to boil it down to things that are distinctive in ME/CFS, not confused by being both cause and effect, and may offer something to think about re putative mechanisms/pathways. I think @yME was right to highlight it.

 

In my opinion you are completely right about this.
Psychiatry and psychology don't study chronic fatigue syndrome, they just study fatigue.
They throw some diseases, without a marker test, together.
Those diseases belong to their field of "expertise", because the GP could not find anything (yet). Must be psychological.
Next they throw in anxiety and depression patients who can also be fatigued, hoping "interventions" will show a bit of succes in any of those completely different groups.
Like the Dutch research. Claiming 6 meters(1%) more in 5 patients,(out of 14) on 6MWT, not confirmed by actimetry, which was swept under the carpet and prof Knoop claims: actimetry does not say anything.
I felt ashamed of being Dutch when I read that. I'll unlearn that.
You can fool some people some of the time, but you can't fool all of the people all of the time.
CBT make fools of themselves.

 

Mainly they conflict with the main diagnostic process in health care: differential diagnosis. For which there apparently is no plan B, only a plan F, in the biopsychosocial model. Which is the root cause problem, a rigid system of rules where if those rules fail, whimsically evil fantasy takes its place. This is why they fail systematically when dealing with common symptoms of illness. This process is simply not meant to work for problems like this, and they won't change the system or have a plan B.

Pretty much the intent behind my current signature. It's a rule that works a lot of the time, and even resembles how machine learning works, with the same overfitting/underfitting pitfalls. But where this rule fails is the places on the maps where there be dragons, and fairies, and weird ghostly things. Not other places and people like the ones that are known, just not known yet. Nope, instead it's the weirdest mystical crap in the modern world, of the exact type that has been left behind through the scientific process. None of which is reasonable, and so not possible to argue with reason.

And it's probably not even accurate to suggest that it probably works most of the time, because there is literally no way to know. We simply don't know how large the set of all diseases and medical conditions is, or what % of those that are 'known' are actually accurate, rather than close enough to be somewhat useful.

At this point it's almost a philosophical problem, about what is knowable and what isn't, and how to deal with the unknown, or even the unknowable, but a quick look at when physicians attempt philosophy, such as Sharpe's "illness without disease" whine, makes it clear this is a complete dead-end that will never solve this problem. Physicians are trained in exactly the wrong way to do philosophy about their job. They are trained as mechanics, on specific makes and types of car parts, and nothing else. There doesn't seem to be any generalizable knowledge in there, every problem is its own unique snowflake where all other problems before don't apply.

They can handle problems not in the manuals about as well as a mechanic could handle a vehicle produced in an alternative universe from a completely different starting set of designs, technologies, processes and components. Or how well a car mechanic from the 1900s could fix a modern electric car. They have a very fixed event horizon outside of which nothing can occur, since they can't see it and give it reality by the simple act of confirming it.

 

So are you saying that if a patient gets PEM from emotional exertion then their illness is partially psychosomatic?

 

IMO the only commonality that can make sense is something that depletes on both physical/muscle and cognitive tasks. Something that is in short supply, is normally replenished quickly, but in our case this replenishing process fails. Like a car engine without a gas tank. It can start working with whatever is in the engine block and the gas line, but as soon as that's burned there is nothing more and it can take a long while for enough fuel to drip through, so it shuts down.

It's the fatigability, not the fatigue, and it has to account for working, poorly, on short order, and failing quickly.

 

The thing is, emotional exertion is very physical. It affects your whole musculature, whether you're laughing, tense with emotional pain, or experiencing waves of anger. It raises your heart rate and changes your breathing pattern, often in quite a profound way.

It's a physical workout, so it's not surprising it induces PEM. It doesn't need a psychosomatic explanation.

 

I think things get tricky if you shift the context of the argument. You could say that tears are psychosomatic because they are caused by feeling sad. In fact in my own experience they aren't directly caused by any feelings because they often appear in situations where one might have sad feelings but doesn't actually feel sad. Once one starts to get into 'mind-body interaction' all the arguments tend to get suspect.

Perhaps emotion being followed by PEM would qualify as psychosomatic but I think the idea of psychosomatic is that it is supposed to explain things beyond connections that seem fairly normal. Emotion is likely to make all sorts of symptoms worse. The question was whether the symptoms worsened as part of PEM are capable of feeding back on to some inner biochemical or signalling process that then created more symptoms. I am just warning that that story sounds very like the BPS cycle and although it is not impossible it has the potential to be unhelpful.

 

I think emotions are easy to plug into the PEM equation, especially strong emotions. Heart rate, respiratory rate etc are all impacted by emotions. Regarding whether "the symptoms worsened as part of PEM are capable of feeding back on some inner biochemical etc...", it's the same as any physical exertion that causes PEM. As to if it might sound like BPS claptrap, and I am certainly sensitive to this, screw them. We're after reality and facts and truth, not the fantasy of a failed logic looking to prop up varied crooked enterprises and regimes.

I'm more puzzled by cognitive exertion causing PEM, although I thought somebody addressed that nicely by noting that when thinking, the brain exerts to different degrees, with the emphasis on exerts.

 

It’s interesting, though, the chronic fatiguability thing. I, obviously, as a severe ME sufferer, have this too, but my eldest daughter, who doesn’t have ME, but a TBI, also suffers from it, albeit from a completely different cause.

Hers is mostly from mental effort and sensory overload, whereas mine is mostly from physical activity but also can affect me from mental overload as well, but she also takes more time to recover from physical effort than a healthy (which she is apart from the TBI) 30 year old woman should. However, she doesn’t get PEM, as you might expect given she doesn’t have ME.

So this might be an example of @Jonathan Edwards “two apparently different causes having almost the same result”.

Edited to add more explanation of my own symptoms.

 

I wasn't saying that physical exertion changes how immunity works; I was saying that exertion causes immune activity: releasing cytokines and other signals. I had the impression that was well-established. When I saw that IFN-g normally rises 24 hrs after exertion, I assumed that was what was causing my PEM symptoms (even though I didn't know about ME and PEM at the time). I didn't come across the delays for other cytokines.

Aren't glial cells constantly interacting with neurons, keeping them functioning properly? It seems logical that altered glial function might alter neural function. I'm imagining a glial cell talking a neuron through some procedure, and saying "Please hold, I have to take this emergency call on the IFN-g line." I know, not scientific, but I thought the question of whether immune signals might be a common factor in most ME symptom worsening due to external factors. It seems common for PWME to have responses--positive or negative--to new infections, immunomodulators, and other things that affect the immune systems.

 

They also involve neurons being active, supported by glial cells, blood vessels, glymphatic vessels, etc. I think there are plenty of possibilities for how emotional responses could trigger ME symptoms. Likewise for cognitive exertion: trying to figure out tax rules involves a lot of neurons that might not normally see much activity. For me, it was abnormal physical exertion that triggered my PEM; a few seconds of unaccustomed exertion would trigger PEM, but hours of accustomed heavy exertion wouldn't. Neurons aren't muscles, but they do adapt to usage.

 

Not true. There's signalling involved, with feedback loops, so it doesn't necessarily require a depletion of a specific type of molecule. Slowing the central clock of a CPU will slow down processing, but I wouldn't call it depletion of clock cycles.

 

Calcium channel blockers - channelopathy ? @duncan

 

@Trish I have been thinking about fatiguability for a few days and questioning why I have a resistance to that description. I need to sit with it for longer. It may be that I have described fatiguability as unusual exhaustion all these years.

 

I think fatigue and fatiguability have as much of a discriminatory faculty for ME/CFS as they do for the flu.