PEM-like descriptions and accounts in non-ME illnesses

[Utsikt]

Well, it wouldn't really fit the name of "malaise", so if only for that reason, it wouldn't seem to fit. But for the reasons I said, I think that is kind of arbitrary.


Just saying that if fatigue+brain fog+vomiting is considered PEM, then vomiting is considered connected to the PEM process, right? It's part of the landscape of associated symptoms. So if there exist people who have even more "malaise-associated" symptoms as part of PEM, it seems probable that there are people with fewer symptoms, such as only vomiting.

I don’t think I have more to add to the discussion above. I can’t get it to make sense within my understanding of PEM.

A forum like S4ME for one. Disability benefits. Support from family and friends because you have a real "scientific" symptom.

But that isn’t the purpose of a diagnosis from a medical standpoint, ref. JE above. Those are just results of how society has organised itself around diagnoses.

Because the diagnosis is arbitrary as it is, and is just describing a heterogenous collection of symptoms. Strict criteria exist for research. If one day, the research finds that those who fit CCC have one condition and those who only have delayed fatigue fit another, then they can be called different things.

I guess it's possible if clinical criteria got watered down, it could seep into research that just uses clinical criteria and add noise. But I'm not sure if any serious biological research is doing this.

See above. The criteria for a diagnosis aren’t arbitrary. They are supposed to catch the people that have «something that is likely to behave in a certain way», so to speak.

 

[forestglip]

Well, I'm exhausted, and I'm not totally sure we're even discussing the same thing, so I'm going to call it for now.

 

[Peter T]

We are in danger of arguing in endless circles about delayed versus immediate PEM. We lack good descriptive data, we really need data on electronic activity monitoring (sorry I can’t recollect the right word) correlated with self reported symptoms and self reported PEM onset and duration. Until we can correlated PEM with an objective biomarker/physiological process, we will need to rely on good observation, a good natural history as it were.

I suspect we have two issues hindering clear discussion:

• firstly our understanding is based on our own experience, unless I am in rolling PEM my experience is that the paradoxical/abnormal state that I label PEM is invariably after a delay, so it is hard for me to relate to what others describe as immediate PEM, though I am willing to to accept that may be my intellectual limitation rather that a reflection of others’ reality
• secondly, given our understanding of PEM is still developing, it is not clear how much we perceive or describe as PEM is influenced by the concept of PEM that we have internalised, for example before I had heard of the idea of PEM I only perceived regular unpredictable fluctuations in my ME, and it was only once I heard of the concept of PEM including the idea of delayed onset that I started recognising a pattern. (Humans are particularly poor at problem solving where there is a delay between the cause and the effect, such as in steering a super tanker.) It could be we are unconsciously editing our symptom profile to fit in with our current conceptualisation, indeed, although now based on food intolerances, sensory hypersensitivities, OI and PEM, I can make sense of, even to some extent predict, my day to day health fluctuations, there is still much that happens that subjectively makes no sense

I think it is important that we focus on what differentiates PEM from fatigue, though fatigue remains a component, also we need to strongly reject the bps trap of confounding PEM with rapid fatiguability. Delayed onset makes it easier to differentiate PEM from rapid fatiguability and I suspect that should stand as a marker for research use, though that need not necessarily exclude immediate onset from any clinical definition. As long as what someone reports as immediate PEM has the similar overall abnormal pattern that distinguishes it from both normal fatigue or from rapid fatiguability, it makes sense to include them both in the same clinical grouping. Indeed I would say that until we have an understanding of the physiological underpinning we have no choice but to consider both PEM.

However if we are asking whether PEM is a feature of other conditions, I would be more reluctant to accept that a PEM phenomenon that only ever occurred with immediate onset as the same as ME/CFS PEM. It is a feature of PEM in ME/CFS that for many it occurs after a delay and if no such delay is regularly, though not necessarily always, observed in the condition being considered I would want to distinguish it from ME/CFS PEM.

 

[Peter T]

Even it vomiting is the only symptom that happens? So you go from baseline fatigue, OI, etc., do an exertion, and then start throwing up a day later, but with no changes to your other symptoms? Is the vomiting then PEM?

I would be very wary of accepting single symptoms as PEM even if there is a delay.

There is more chance of other explanations. With the vomiting for example, migraine and vomiting are part of my PEM experience, but they are also part of my gluten intolerance, which also has a twenty four hour delay in symptom onset. It is impossible to always be certain which is which, certainly before I was aware of my gluten intolerance I was attributing its effects to my ME. I could envisage if my ME had resolved but my gluten intolerance remained when I was ignorant of the existence of that intolerance I would misattribute ongoing symptoms to ME/CFS. (Especially as eating gluten, eg sandwiches and pasta, tended to happen more when I was too busy/fatigued/unwell to cook properly.)

 

[richie]

But literally 50+ % of the population is likely to have delayed fatigue or muscle soreness after exertion.

I don’t see a world where that isn’t going to do the exact thing the “CFS” label did to the clinical construct

My experience of muscle soreness has always been "lactic or muscle damage" type during exercise, consistent , I suppose, with low anaerobic threshold, from a boy. Whether this was really a form of allodynia in the presence of normal muscle metabolism, I don't know. Fasciculation and formication was experienced before ME?sarcoid?Lyme but only as I remember following hard exercise after a few months of no exercise. i.e.. first football at school after summer holidays. This always passed by 2nd game and was once ayear.

Muscle soreness with fasciculation and formication and tired legs after , say, a 25 yards walk was a phenomenon from 1988 and I would not liken it to any previous (post or during) exercise phenomena except perhaps the transient football related stuff at school. I would not say that my experiences pre 1988 were like those previously. I accept that any of these phenomena in themselves do not amount to regular descriptions of PEM, though there may be uniting underlying biological aspects. In any case the exertion intolerance I have in ME was not normal post exertion fatigue/soreness.

Muscle soreness and delayed fatigue in normals should not be considered in principle except as controls, since they are well and therefore have nothing to do with definitions in ME. But there may be value in studying presumed EI , PEM senso lato and sensu strictu and seeing what they have in common and what distinguishes them. IMO labels should come after if we are elucidation underlying biology which must be foundational for a scientific assessment.

 

[poetinsf]

I still feel that definition before investigation is cart before horse,

That may be, but we still need to define the problem in order to investigate the problem. You'd be just kicking the tires around otherwise. It could well be a reiterative process of investigating - learning - redefining as you said, till we get the full picture. And starting the gradient walk from a conservative point is usually a better strategy. Unless you are reasonably sure that two different manifestations are the same phenomenon. We know, for, example, severe and mild cases of ME/CFS are two different presentations of the same because patients go from severe to mild and vice versa all the time. So it would be prudent to include both severe and mild cases in investigation for more complete picture. PEM with or without delay, on the other hand, we are not so sure at this point.

It's different clinically, obviously. The aim there is to provide treatment and reduce the suffering rather than figuring out what it is. So, it would be better to be liberal than conservative there.

 

[Mij]

Almost 'recovered' mild/moderate pwME experience serve delayed PEM when they cross that fine line. Agree, all groups should be studied.

 

[richie]

That may be, but we still need to define the problem in order to investigate the problem. You'd be just kicking the tires around otherwise. It could well be a reiterative process of investigating - learning - redefining as you said, till we get the full picture. And starting the gradient walk from a conservative point is usually a better strategy. Unless you are reasonably sure that two different manifestations are the same phenomenon. We know, for, example, severe and mild cases of ME/CFS are two different presentations of the same because patients go from severe to mild and vice versa all the time. So it would be prudent to include both severe and mild cases in investigation for more complete picture. PEM with or without delay, on the other hand, we are not so sure at this point.

It's different clinically, obviously. The aim there is to provide treatment and reduce the suffering rather than figuring out what it is. So, it would be better to be liberal than conservative there.

I would say dividing PEM by onset type might be an approach, allowing one focus on a ypically post 12 hrs onset cohort and another focus on those with a typically earlier onset. maybe starting at the extremes where difference is presumably most likely to show and then moving into the muddled middle. That would render more data and cater for numerous concerns.

 

[poetinsf]

The more I reflect on it, the more I'm realizing that I probably had a long "prodromal" phase which was primarily characterized by "rapid fatiguability" and fluctuating baseline fatigue.

Great, I learned a new word today! I don't think this is an uncommon experience. Bruce Campell talks about how he struggled with fatigue prior to the onset of flu-like sickness that didn't go away (and how he managed to get out of it by cutting back by 10%). So did Dean Anderson and Jamison Hill. I myself was struggling to have 2 good days out of a week. I remember spending quite a bit of time lying down back then even though I was able to weight-train without any adverse effect. These cases look like something snapping after a chronic stress.

 

[V.R.T.]

The more I reflect on it, the more I'm realizing that I probably had a long "prodromal" phase which was primarily characterized by "rapid fatiguability" and fluctuating baseline fatigue. It was only in retrospect that I realized my worst fatigue days were always following the days where I overdid it and weren't actually random. So either something "switched" over when I started experiencing typical PEM, or maybe there was just an increase in intensity of the underlying problem such that the same amount of activity triggered faitgue+everything else whereas previously it was only fatigue.

I think it's also interesting to compare to the symptom pattern for most common viral illnesses. I think the typical onset tends to be something like:
1) feel tired for no good reason for a day or two, write it off as bad sleep
2) wake up with a sore throat/fever/malaise/etc. and retroactively realize that the fatigue was the first sign of infection

Which presents an interesting story of some immunological cascade that has different presentations based on either some stepwise progression of signals, or based on increasing concentration of one particular signal (or both!).

I've been idly wondering if it is actually the same cascade in PEM vs. viral infection, it's just that pwME don't really register the 1st fatigue phase because that's already our baseline. So for us it can seem like "I do activity one day, I feel normal the next, and then I feel like I got hit by a truck on the third day"

I've discussed this elsewhere but I think I had a prodromal phase of about 6 years. Although sometimes I think about certain details, like the fact my hangovers tended to get nastiest almost exactly 12 hours from my last drink rather than as soon as I woke up, and how much sicker I tended to feel at/after music festivals, and I wonder if I didn't already get PEM to some degree.

But I do remember feeling just a lot more tired and foggy at age 19 onwards than at 18. With noticeably less pep in my step than my peers. And I had disturbed/reversed sleep and other things.

I wonder if it's the case that a certain amount of immunological 'hits' can land you in an in-between state between good health and ME/CFS. And then a few more launch you into full blown ME.

 

[mariovitali]

I wonder if it's the case that a certain amount of immunological 'hits' can land you in an in-between state between good health and ME/CFS. And then a few more launch you into full blown ME.

Or perhaps also metabolic hits such as environmental toxins and even certain medications

 

[Utsikt]

Or perhaps also metabolic hits such as environmental toxins and even certain medications

That just sounds like another way to hit the immune system, though? All roads lead to Rome, etc.

 

[mariovitali]

@Utsikt I don't understand your reply to be honest. In case you believe mecfs is strictly of viral origin then you should reconsider by looking at the known triggers

 

[Utsikt]

@Utsikt I don't understand your reply to be honest. In case you believe mecfs is strictly of viral origin then you should reconsider by looking at the known triggers

I don’t believe that ME/CFS is strictly of viral origin. The original comment talked about hits to the immune system.

Environmental toxins and medications might affect metabolism, but you can almost be certain that it will interact with the immune system.

 

[Formerhuman]

I'd like to understand more clearly what is the current opinion of patients and advocates here on presence of PEM in other diseases. For example, some people with multiple sclerosis report PEM in their Reddit community. Do you agree with the assumption that PEM is not specific to ME/CFS?

 

[Jonathan Edwards]

For example, some people with multiple sclerosis report PEM in their Reddit community.

I would be very wary of this sort of discussion on social media. We now have everyone saying they have brain fog because Long covid has made brain fog fashionable. Medical terms carry all sorts of subtle caveats in the way they are used by doctors in diagnosis. PEM for me means a particular temporal pattern of the symptoms of ME/CFS. Someone with MS may feel awful having done too much but that usefully fall under PEM. (Moreover, people on social media who have been told they have MS may not have it after all.) I think these debates go nowhere. It doesn't matter when it comes to making a practical diagnosis.

 

[Peter T]

I am not saying that PEM is unique to ME/CFS, but I do feel that we have not yet adequately confirmed that it occurs in other conditions.

As we have often raised here, a big problem is that many people including some ME/CFS researchers confound it with more rapid fatiguability that does occur in many conditions, including ME/CFS and MS.

 

[Mij]

The 'cog-brain' in MS certainly describes my cognitive difficulties, but it doesn't necessarily involve exertion so I wouldn't describe it as PEM related.

That being said, I experience the same 'cog-brain' during delayed PEM ¯\_(ツ)_/¯

 

[Kitty]

I do feel that we have not yet adequately confirmed that it occurs in other conditions.

Yep. And whether the answer's yea or nay, it'll still be something we don't understand, can't measure, and struggle to describe.

 

[Formerhuman]

I’m asking about this because some people argue that ME/CFS isn’t a distinctive condition, since PEM is allegedly present in other diseases.

Here’s a quote from a Reddit account with diagnosed multiple sclerosis:

"I knew my fatigue and knew my limits. But recently it seems like even light physical activity (which i totally tolerated before) causes me to crash with total exhaustion, muscle pain, tingling sensations and unrest. Basically its unimaginable of functionning as a normal human being even though I have no obvious neurological deficit. Crashes occur within a few hours delay, peak after a few hours and subside within a day. Basically light jogging for 10 minutes ruines my entire next day. What are the chances of this being attributable to ms (a relapse maybe) or is this something else (pseudo-exacerbation)? Bloodwork turns up normal and I got no other symptoms of infection or something else. It rather matches descriptions of post excertional malaise in chronic fatigue syndrome. Absolutely not looking forward to another medical challenge right now..."



However, I’ve also seen many people with MS on Reddit say they can exercise successfully. That makes me think that the post-exertional worsening some patients describe isn’t the same as in ME/CFS and probably relates instead to so-called pseudo-exacerbations and Uhthoff’s phenomenon.

Sjogren’s is less clear to me. I haven’t found a good description of post-exertional worsening on the Sjogren’s subreddit. Some people with Sjogren’s claim to have PEM, and some of them developed PEM after COVID.