Were historic 'ME' outbreaks really ME?

I think we're getting too caught up in this idea of a 'viral attack of the nerves'. Just because that wasn't the case doesn't a) mean there wasn't a viral trigger in these cases which evolved into ME, or b) mean that McE and B were right.

 

To some degree that would be the case, but only if the doctors making the notes very inexperienced in neurological examination. The problem we have is that may be the case. But presumably Ramsay had to goon the basis of the same observations. If he examined the patients himself and came to a different conclusion then he should have recorded that in the records.

We are left with the basic problem that there does not seem to be a record of a competent neurological examination with a well considered anatomical diagnosis of a lesion. Maybe there is somewhere else but then why did McE and B not know that?

There is also a limit to the extent to which we can put self-image patterns of symptoms down to the person recording them. The glove and stocking patterns might be poor documentation biased by the idea of glove and stocking neuropathy but hemianaesthesia affecting arm and leg but not body is unlikely to be made up that way. And even medical students are taught early on that symptom cut off where limbs join body is a fairly reliable indication of no neuropathology.

 

I am not sure what to call it. I would not want to call it anything just from the records. All I think one can say is that these patterns are often enough seen and on investigation do not relate to specific nerve damage. Presumably they arise higher up in the brain but that is about all one can say. They do not make sense in terms of the types of viral attacks on nerves we know about and nor do they make sense in neuroanatomical terms, whatever the cause.

Glove and stocking neuropathy exists and is common enough but the reason for doubting that this is what was present is that all the charts of sensory loss look much the same and of a degree that is actually quite unusual in real glove and stocking neuropathy, which is not quite like the name suggests.

 

My impression is that this IS what was being called ME, at least by Acheson and co. And it seems pretty certain it was not an encephalomyelitis. There wasn't any other illness called ME that did actually have encephalomyelitis as far as I an see.

 

I think Ramsay is right to point out that in each of these outbreaks there was an epidemic of some sort of feeble viral illness. But I am not sure that McE and B were denying that. The question is whether or not the apparent neurological signs were real signs of some specific neurological abnormality. The ones McE and B describe look unconvincing. Ramsay does not comment on these but focuses on ocular and facial palsies.

I have not yet seen any detailed description of cranial nerve signs. I would be surprised if ocular palsy occurred in 43% of the two hundred odd cases. Ocular palsies are not common even amongst conditions that produce cranial nerve lesions. Maybe some really unusual virus was involved in this outbreak but it would have to be very unusual and no longer relevant because if we were still seeing ocular palsies in this sort of number it would be firmly in the textbooks. ME as we know it today has nothing to do with ocular palsies and probably nothing to do with facial palsy.

I am very much in agreement that we have been left with the impression that all ME has been shown to be hysteria. And that is a disaster. But it seems to me that it causes no problem to anyone to accept that McE and B may have been right that the so-called neurological signs of that led to the name ME were mostly due to panic about having an unidentified polio-like illness. As long as everyone agrees that what we call ME now is a chronic condition that has nothing much to do with whatever acute illness happens to set it off.

 

There is also an account by Byron Hyde (whose work I am honestly not v familiar with) meeting with McEvedy in later life and McEvedy admitting they had not actually seen patients. Again this is anecdote and I am too tired to find it right now, but another interesting strand.

 

Forgive me for wading in here without any real science background but I have just one brief thought.
Is it possible that what happened to the patients being referred to here is that they experienced a messed up electrolyte system (as a result of an acute infection) that manifested in all these symptoms that would be viewed as neurological in origin?

So (to put it another way) is it possible that symptoms that 'look' neurological are not (neurological) because some other bodily system is producing them?

ETA: (neurological) for clarity

 

That is what Charcot said, ironically, about those he later termed hysterics. What changed in his case is he became enamoured with mesmerism. Its entirely reasonable to infer possible neurological damage or dysfunction. The issue is some, usually psychiatrists, make the leap from unknown cause to psychiatric cause. That is what happened with McEvedy and Beard and the current psychobabble group. If they just left it at unknown then the damaging impact of their ideas would be greatly reduced.

 

Found it: http://www.imet.ie/imet_documents/BYRON_HYDE_little_red_book.pdf

Pages 15,16

 

Kind of. Many of the symptoms might be neurological but have metabolic or immune causes, just to name two.

 

So then it seems to me to be entirely unreasonable for McE & B to immediately have jumped to the conclusion of a conversion disorder. But also to be fair we are talking about their opinion formed from decades ago. It seems that this continues to be the default (psychological) regardless of whatever 'modern' age is being discussed because there will always be illnesses that defy understanding due to limited investigative technologies and so much as yet unknown (certainly with regard to metabolic or immune origins).

Yet somehow, now having been on the receiving end of a momentously stupid lack of critical thinking on their part I can't help but think how terribly obvious it is that their thinking is fatally flawed.

 

Following Hutans thought and taking things further off thread still: I think a group of post Ebola, post SARS, post Polio and PWME people would make a very interesting study - I'd love to know where their symptoms overlap with ME-CCC/ICC and dont, and how potential biomarkers differ between groups/what we have in common.

I am more or less an idiot these days what with no science background and precious little memory and no ability to hold complex models in my head or multitask. Perhaps someone can explain to me why this sort of study is unlikely to shed any light on anything useful.

 

I guess typical glove and stocking neuropathy is also more common in chronic conditions/exposure to toxin/virus and comes on over a longer period of time (diabetes, alcohol, vitamin deficiencies, hypothyroid, autoimmune diseases etc) and affects peripheral nerves rather than CNS?

So is the logic that the time frame was too short after infection? ...I tried to check it out but couldn’t find anything on typical times for this to develop post infection?

 

There was usually a flu-like, gastrointestinal or vertigo-like illness. Then, a few weeks later, you'd start to see other symptoms such as the muscle fatiguability and supposed neuro signs.

My feeling on this, however, is that if ME is indeed either a signalling problem or a metabolic trap, this might indeed come on overnight. And many of us do feel that way; like a switch was flipped and we became ill.

Neurologists did look at patients at the time, as did psychiatrists, and hysteria was rejected in each outbreak by those investigating.

That doesn't mean we have conclusive evidence, and I get that, but McEveady and Beard made conclusions that weren't supported by the outbreaks. Was a polio panic present at each and every site? Maybe. It seems unlikely, but I'll admit it could have skewed results. But I don't think that accounts for the outbreaks, either.

Look at Gulf War illness, as an example that's similar to ME but which was always put down to hysteria or stress for the same reasons. In the last 14 years, researchers have recorded shrinkage of the cortex (about 5%), and the three main proposed subgroups are based on where the lesions or dysfunctions are thought to be (brainstem, basal ganglia, or both). Yet these same areas and similar brain changes are suggested in studies for ME.

 

No, true neurological signs - meaning patterns of symptoms and bodily appearances that actually indicate nerve malfunction - can arise from all sorts of things like electrolyte disturbance (calcium, magnesium whatever). They still reflect the way individual nerves or neural tissue regions are malfunctioning.

The signs that McEvedy and Beard discuss do not look as if they indicate specific nerve malfunctions. They look more like disturbed interpretations by the brain of subjective sensations. As McE and B point out, we all have such disturbed interpretations at times.

 

McE and B make it clear they never met the patients. I think that is the strength of their analysis. They went purely by what was in the records - the information available to Ramsay. It seems they focus on only some of the features but they do not hide this. They focus on features that are described in enough detail to analyse retrospectively, like patterns of sensory symptoms.

It is interesting that the neurologist warned Ramsay against letting others see the records. If the neurological findings were well documented there would be no reason to be concerned.

 

In a neurological examination you end up inferring neurological lesions based on consistent evidence. So you infer an L5 root lesion if the sensory loss is confined to the top of the foot (not the sole) and there is weakness of extensor helices longus. If there is no sensory loss but there is more general foot muscle weakness you are more likely to infer a distal myopathy - and so on.

The problem with the patterns shown in McE and B is that they do not really fit with any neurological domain. As a junior registrar I did not appreciate the significance of this. However, after six months of neurology training I came to realise that if one is careful one can more or less always identify which domain of which tissue is affected. A registrar who did not come to the right conclusion when presenting the case to the boss would feel he had better not be so sloppy next time. If the symptoms are inconsistent with any domain one can be pretty sure no neurological lesion will be found on electrical or other tests.

Itmight be thought that McE and B were coming to the conclusion that these were not true neurological signs because they were psychiatrists. But this is not the case. A trained neurologist would agree with their analysis. Whether 'hysteria' is a useful alternative 'explanation' is another matter.

 

Yes, admitting was wrong word, I was half asleep when I wrote that. I meant stating or saying - still the Byron conversation is interesting. But again is anecdote. I am just glad I have never had to face a McEvedy or a Beard-type. Onset of my illness was only ten years after their paper.

 

I think this is a relevant and interesting question. The significance of the 'outbreaks' for the study of ME really relates to whether or not they are due to specific microbes that have a high likelihood of triggering ME. And that has got confused with the nature of the acute illness. It seems that EBV and Q fever give high rates of ME. It might just be the level of initial febrile response that matters. EBV produces one of the worst with fever up to 40 for days. But it might be to do with microbes that get inside cells involved in immune signalling or something like that. Ebola certainly seems interesting.