Were historic 'ME' outbreaks really ME?

[AR68]

This thread has been split from https://www.s4me.info/threads/bmj-pressure-grows-on-lancet-to-review-“flawed”-pace-trial.5444/page-6




They seem to play these word games all the time. I have been trying to work out the attitude to "hysteria". In their book Wessely, Hotopf and Sharpe say @p232 10.5 CFS and hysteria:

Thus hysteria, used properly as meaning conversion disorder, is rarely a tenable explanation for CFS. Three caveats are necessary. First in the context of epidemic forms of ME, explanations involving transmitted emotional distress ("mass hysteria"), merit attention. However, as we and others have also shown, such examples have little to do with CFS. Second...…"

My interpretation of this is that they confirm their apparent approval of the views of McEvedy and Beard for the epidemic forms, but clear themselves by saying that such cases are not CFS. I would be happy to have alternative views should others think me wrong. It seems like a case of Humpty Dumpty Syndrome-words mean what I want them to mean.

Given that the term 'Myalgic Encephalomyelitis' comes from the RFH in 55 (I've simplified it somewhat) any diagnostic criteria should really come from that. I understand that it's slightly more complicated than that.

Obviously certain nameless people subsequently adulterated all that.

Just to add that I believe that David Tuller may have something to say on the RFH in the not too distant future....

 

[chrisb]

Given that the term 'Myalgic Encephalomyelitis' comes from the RFH in 55 (I've simplified it somewhat) any diagnostic criteria should really come from that. I understand that it's slightly more complicated than that.

That's my view also. I thought it was a basic principle of taxonomy that the earliest description stood. If you want to vary the description you have to vary the name, to make the relevant description clear, although that practice in botany makes the gardener's life a nightmare.

 

[adambeyoncelowe]

No acute illness can be said to be 'ME'. ME is what happens afterwards. I think even Ramsay (and people like Hyde now) would say that, too.

What complicates matters is that Ramsay sometimes described the outbreak and the chronic illness as if they were the same thing (hence 'outbreaks of ME'; which could only ever really be 'outbreaks that lead to ME'), but in other cases was clear that the initiating viral trigger merely set the whole thing in motion.

Now we might term the immediate symptoms 'post-viral fatigue syndrome' and differentiate that from ME, which is the 'chronic' phase (i.e., what we talk about after that six-month period has elapsed).

 

[Trish]

Given that the term 'Myalgic Encephalomyelitis' comes from the RFH in 55 (I've simplified it somewhat) any diagnostic criteria should really come from that. I understand that it's slightly more complicated than that.

That sounds to me like a description of a work of art which, rightly, should not be painted over and turned into something else.

But medicine is not like that. Knowledge evolves. A name that is given to a condition first described in a particular area by a particular doctor might turn out to be a subgroup of a more widely occurring disease, or even a rare or unusual presentation of an already known condition. If we try to keep definitions set in stone, everyone who fulfilled Freud's definition of hysteria should still be diagnosed as hysterics.

Or have I misunderstood? I often do.

 

[Jonathan Edwards]

I thought that was the proposition to be proved.

I think that proposition is pretty sound. An acute febrile illness with apparent neurological signs suggestive of neuropathy, monoplegia, ocular and facial palsy bears no resemblance to the chronic syndrome of ME.

 

[Jonathan Edwards]

Given that the term 'Myalgic Encephalomyelitis' comes from the RFH in 55 (I've simplified it somewhat) any diagnostic criteria should really come from that. I understand that it's slightly more complicated than that.

Obviously certain nameless people subsequently adulterated all that.

Just to add that I believe that David Tuller may have something to say on the RFH in the not too distant future....

Medical terms change their meaning with time just like other words in a language.
Myalgic encephalomyelitis does not actually come from RFH but from a shared speculation by certain infectious disease physicians and epidemiologists that there might be a new febrile illness with neurological features to separate out from those already known. The test of time indicated that that speculation was probably groundless. In the 1977 edition of Brain's Diseases Of The Nervous System, which was one of the most exhaustively referenced texts of its time gives detailed sections to Coxsackie-based illnesses but makes no mention of myalgic encephalomyelitis.

So ME as originally defined turned out to be a category of no value. However, whereas people like Acheson were chiefly interested in the acute illness, Ramsay was also interested in what we now call ME and the problem is he treated them as if they were one concept, which they are not. So the term changed meaning. One could say that is too confusing and stop using ME, which is exactly what much of the medical profession have done, but the term has stuck as a term for the chronic illness and has some advantages over chronic fatigue syndrome.

 

[Jonathan Edwards]

No acute illness can be said to be 'ME'. ME is what happens afterwards. I think even Ramsay (and people like Hyde now) would say that, too.

As I understand it that is not what the term was coined to mean. Ramsay did not coin the term. And as you say, Ramsay muddles the two up.

 

[duncan]

acute febrile illness with apparent neurological signs suggestive of neuropathy, monoplegia, ocular and facial palsy bears no resemblance to the chronic syndrome of ME.

It does to neuroborreliosis.

Of course, Lyme Encephalomyelitis is a well-known phenomenon. What perhaps is lessor understood is what happens to Lyme Enceph patients who go untreated or undertreated? More to the point, why should this not be relevant to other diseases whose neuro impacts are less clear once they trend chronic?

I have an additional question: why must neuro-symptoms correlate with lesions? Must lesions even be present for neuro symptoms to manifest? Does the absence of one preclude the other? I am pretty sure we don't need lesions for there to be conclusive evidence of different cranial neuropathies.

 

[Jonathan Edwards]

why must neuro-symptoms correlate with lesions? Must lesions even be present for neuro symptoms to manifest? Does the absence of one preclude the other? I am pretty sure we don't need lesions for there to be conclusive evidence of different cranial neuropathies.

Neurological-type symptoms often occur without evidence of a nerve lesion. But if a pattern of symptoms has not been found to correlate with evidence of a nerve lesion on objective investigation then there is no reason to use it as an indicator of such a lesion. So I am not sure the point of your questions.

Conclusive evidence of a cranial neuropathy is conclusive evidence of a nerve lesion because that is what is meant by a cranial neuropathy - a cranial nerve lesion. I am not sure what else you are thinking it means.

 

[chrisb]

I suggest that Ramsay was merely picking up and emphasising a different aspect of Acheson's description:

Relapses have occurred in almost all outbreaks. In eleven of the fourteen epidemics symptoms which suggest activity of the disease have persisted for months or for years in a few cases...…..

 

[duncan]

Conclusive evidence of a cranial neuropathy is conclusive evidence of a nerve lesion because that is what is meant by a cranial neuropathy - a cranial nerve lesion.

This is not the same as saying you must have an observable lesion to have a cranial neuropathy. I have an NIH-diagnosed cranial neuropathy with no identified lesion, unless I am confusing my terms, which is certainly possible.

 

[duncan]

But if a pattern of symptoms has not been found to correlate with evidence of a nerve lesion on objective investigation then there is no reason

I'm sorry. I thought you were trying to make the point earlier that neuro symptoms are hard to justify without evidence of lesions. Perhaps I was mistaken.

 

[Wonko]

From an outside, and entirely unqualified, position it appears that (based on what's been posted here);

Neurology is defined as problems caused specifically by lesions, and it therefore follows that if no lesions can be found it is, by definition, not a neurological problem.

Reference has been made to many other things that look like they are neurological, but as no lesions have been found after closer examination they are therefore not neurological in origin - the common response to which is to say there are NO neurological issues and refer on to MH.

Rather than try and figure out what the problem actually is, simply decide it's not neurological and refer on.

(possibly, apparent definition aside, neurology should aim to fix issues with the nervous system, rather than just identify lesions?)

 

[Jonathan Edwards]

the common response to which is to say there are NO neurological issues and refer on to MH.

This may be a reasonably common response but I thinking the vast majority of cases the response is more sensible. It is that if there is no evidence of lesions in the parts of the nervous system where we understand clearly the relations between structure, connections and function then we have to assume that the symptoms arise from problems at a level where we do not understand those relations so well - which applies to a lot of what goes on in the cortex. If we have no reason to think these are associated with the sorts of problems psychiatrists deal with - like low mood, schizophrenia, etc. then the standard response in the neurology department I worked in was to admit that one did not know what was the cause but that in the absence of problems suggestive of progressive damage, like MS, one might be able to reassure.

Medical specialities never really fall under watertight definitions. It is always a matter of trying to deal as best one can with whatever one has experience with and to refer elsewhere if one has reason to think someone else will do better. There is no doubt that ME has fallen through the gaps in the system though.

 

[adambeyoncelowe]

From an outside, and entirely unqualified, position it appears that (based on what's been posted here);

Neurology is defined as problems caused specifically by lesions, and it therefore follows that if no lesions can be found it is, by definition, not a neurological problem.

Reference has been made to many other things that look like they are neurological, but as no lesions have been found after closer examination they are therefore not neurological in origin - the common response to which is to say there are NO neurological issues and refer on to MH.

Rather than try and figure out what the problem actually is, simply decide it's not neurological and refer on.

(possibly, apparent definition aside, neurology should aim to fix issues with the nervous system, rather than just identify lesions?)

I may be wrong too, but I came to a slightly different understanding.

I think the point is that some neurological symptoms imply a lesion. If the lesion isn't there, then the neurological symptom probably isn't, either.

Meanwhile, other symptoms appear to be neurological, but might be explainable by other methods.

So what we have is a list of symptoms from outbreaks that don't show the required lesions you'd expect, or may not actually be neurological in nature. In addition, some of the symptoms recorded seem to imply the opposite of objective neurological findings (i.e., they appear to be due to suggestion).

More generally, I think things like channelopathies are considered neurological, but they don't necessarily involve lesions. So I don't think neurology requires lesions in every case. But that still doesn't make the list of symptoms we do have from those outbreaks any more accurate.

Hence, ME may still be neurological, but because it involves signalling problems or a channelopathy, not because it involves clearly identified lesions. The outbreaks don't seem to show neurological lesions or a virus that attacks the nerves, as claimed.

 

[Jonathan Edwards]

More generally, I think things like channelopathies are considered neurological, but they don't necessarily involve lesions.

A lesion just means a physical abnormality of a particular domain of tissue. So if a channelopathy is producing symptoms there is a lesion somewhere, even if the term might not be used in that context very often - because the abnormality may be very diffuse.

To say there is a lesion of a cranial nerve does not require that you can see something on a scan or electrical testing. Clinical examination is considered reliable enough to say that there is a lesion if the nerve is not working - your face droops in a specific way or you have vertigo under specific conditions etc. So a cranial neuropathy is a cranial nerve lesion - they mean the same. If you not sure it is one you are not sure it is the other. You may not be sure of the cause or detailed structural change but that is not required for either diagnosis.

The problem with the apparent signs that McE and B analyse is that they do not provide strong evidence for any specific lesion. Nerves do not work in such a way as to give those patterns.

 

[duncan]

Another consideration is that some lesions resolve with abx, and yet neuro issues may persist.

Incidentally, channelopathies frequently do not readily manifest in any overt physical abnormality other than that is reported by the patient. If lesion is to imply any physical abnormality, whether or not it is observed, perhaps medical lexicon needs to change. I know many clinicians and researchers who are misusing the term, if @Jonathan Edwards is correct. For the sake of accuracy and coherency, perhaps a different term can be substituted.

 

[Obermann]

I think it is quite clear that the meaning of the term ME has shifted, and that it originally referred to an acute illness with a strong propensity to trigger the chronic syndrome that we now refer to as ME/CFS.

There were many outbreaks of the acute polio-like illness. Although the agent(s) was never identified, there is evidence that it was infectious in nature. It was transferred to rhesus monkeys in animal experiments in Australia (Pellew et al, Med J Aust, 1955). Children in Iceland in regions that were exposed to epidemic ME showed a different immunological response to polio vaccine than other children (Sigurdsson et al, Lancet, 1958). There also seems to have been interference with polio in some epidemics. The Icelandic coastal polio epidemic in 1955, for example, never penetrated regions that had been exposed to epidemic ME a few years earlier (Sigurdsson et al, Lancet, 1958).

Initial reports suggested that most patients recovered (Pellew, Med J Aust, 1951), but it was soon recognized that the illness had an alarming tendency to become chronic (Sigurdsson, Lancet, 1956; Ramsay, Postgrad Med J, 1978). It seems that the focus shifted from the acute illness to the chronic syndrome in the 1980s. ME was listed under the heading “Inflammatory diseases of central nervous system” in ICD-8 (1969) and ICD-9 (1978), but under “Other disorders of the brain” in ICD-10 (1994).

It is unfortunate and confusing that we use the same name for the acute illness and the chronic syndrome; in particular since the latter can be triggered by other agents than epidemic ME, as demonstrated in the Dubbo study.

 

[Mithriel]

Just a few thoughts.

McE and B wrote their report fresh from their triumph describing 2 different epidemics of "hysterical vomiting" in girls' schools. They were obviously mass hysteria because younger girls became ill when they saw older girls throwing up and we all know that only a faecal/oral route spreads that (sarcasm, norro, curse of the wards) They were looking for another case of mass hysteria among females and lit upon the Royal Free. Ramsay said they used records of people he had not considered to have the disease. His colleague told him he should not have given a blanket release for the records because he suspected the motives of the researchers not because he felt they would find out what was in them.

Mass polio vaccination has changed the character of enteroviral disease so it is not surprising that they do not show up the way they did at the Royal Free.

The Royal Free is on several different sites. I read an account written by a nurse who became ill. She said that they heard rumours that a lot of medical staff were going down with flu (not polio) before they were transferred to the main hospital as they were short staffed as so many had been admitted.

I am very dubious about neurology. The brain is infinitely complicated yet it is considered that a few tests will show up everything that can go wrong. If you look at how many things were "known for a fact" that have been changed from the impact of lesions of the spine (only some were meant to give paralysis, I can't remember the details off hand) to the immune system being the only system of the body that was not under control of the brain (Two outsiders who had not been told this "fact" discovered the connection) it has a bad history of mistakes.

Ramsay saw ME as similar to polio in that the disease was the chronic effect of the infection. If we do not separate polio from the infection when we talk about it I do not see why we have to with ME.

My own disease was neurological, or brain based if you like. I never missed a day of school, but I had episodes of paralysis, foot drop, loss of speech, vision problems, absence seizures, inability to pass urine. I was deeply ashamed of these and hid them as much as possible.

When you read about functional neurological disorders, you realise how divorced neurologists are from science and medicine. They haves passed on too many "truths" When we know about things like blindsight to dismiss certain seizures as hysterical becasue people do not burn themselves on cookers, well. Hysteria by its many names has been taken as an answer so they have stopped looking for problems in the brain.

 

[alex3619]

Addressing the new thread topic, when I looked through many of the outbreak reports some years ago, I was struck by how different the symptoms were. To me it looked like the triggers were different. I am unsure to what degree we can compare one cluster outbreak to another, unless it was close by both geographically and in time.

On neurological factors I think its abundantly clear there is a neurological impact. The issue is that it is not properly understood. We don't know if its primary or secondary. We are trying to assess unknown unknowns.

The brain is infinitely complicated yet it is considered that a few tests will show up everything that can go wrong

I would not say the brain is infinitely complicated, but it is the most complex thing science has ever investigated, and our investigative tools are still severely inadequate to the task.

I want to make clear these two claims are different, and only one is reasonable -

1. We can possibly infer a neurological problem in ME.
2. We can infer a possible neurological problem in ME.

The second one accurately reflects the uncertainty, including the unknown unknowns. The first one does not. Neither allows for definitive diagnosis.

I think there are subsets who clearly, and definitively, have neurological issues. We cannot however generalise this to say exactly what is happening in everyone.

I am still struck by the 1955 finding that blood from ME outbreak patients cause spinal lesions in monkeys. Its hard to say about humans, but we know that some of us do have spinal lesions on autopsy. Sadly we have so little data on this that the prevalence of spinal lesions is largely a guess.

If Stanford replicates it structural changes findings then we have strong evidence of structural changes in the ME brain. They might do that, they might find otherwise. We have to wait.

Classical neurological exams are looking for classical problems. ME does not fit that. That does not mean that ME does not have neurological issues, only that if it does we do not understand them yet. It took a long time for brain dysfunction and damage in MS to be understood, and I am not sure its properly understood even now.

It is fair to say we have no proven neurological damage in ME. It is not fair to say there is no evidence of damage, or that damage could not exist, just that its not proven yet.

One thing we need to explain with regard to ME outbreaks is why they appeared to stop. I am not sure they did. I suspect they got a different diagnosis. I suspect they are now identified by triggering factors, like Giardia or SARS. I suspect one justification for this is the symptomlogy and outcome are different for each trigger, leading to the idea that they are different. Again, they might be, or might not be. Now we are starting to understand the conserved biological response to severe infection, I think we need to consider each case from the perspective of both the trigger and the response to that trigger, together.