Were historic 'ME' outbreaks really ME?

arewenearlythereyet said:
I guess typical glove and stocking neuropathy is also more common in chronic conditions

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?
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Glove and stocking neuropathy is not uncommon as an acute illness - in vasculitis for instance.
 
Jonathan Edwards said:
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.
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ETA: I've only just seen the last few posts. I'm guessing the febrile nature of some viruses might account for these symptoms, then? Like how signals are reduced in brains of MS patients when they get too hot?

What could be the explanation for these symptoms? Fleeting disturbances of subjective experience caused by a virus, perhaps overlaid in some cases with panic over polio-type illnesses? Mass hysteria does seem very unlikely, and I'm not sure we can reasonably assume every investigating medical team made exactly the same mistakes years and many thousands of miles apart, either, but I accept that there isn't any objective evidence of a localised lesion.

I'm curious if any of this fits a model of brainstem or basal ganglia disturbance? If not, how would issues in those regions affect the symptom profile? Would we expect specific things that weren't readily apparent in these outbreaks?

The reason I ask is that these regions keep cropping up, not only in ME, but also in Gulf War illness. In the latter, there's presumably chemical damage to the brain, which seems (mostly) unlikely in ME, but could signalling issues arise that cause similar symptom profiles? (VanElzakker suggested that the brainstem region is where the brain 'samples' circulating cytokines, and that if those are present in the blood, they would also affect the brain through this point of contact. So that might explain how similar symptoms happen in both illnesses, but without any objective damage in ME.)
 
adambeyoncelowe said:
Was a polio panic present at each and every site?
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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.
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I suspect a polio panic was present every time a patient came in to hospital with a fever and neurological symptoms in the 1930s-50s. Most other infections had become manageable by then but polio was still a concern to all parents in 1955. My wife was not allowed to swim in public baths because her father was a doctor and feared she would get polio. Infectious diseases were what worried people in those days, rather than slumps in the stock market.

I agree that it looks as if both Gulf War Illness and ME may involve some long term structural or physiological change to brain stem, basal ganglia or cortex. But that would not fit with ocular palsies, glove and stocking sensory symptoms or monoplegias.
 
adambeyoncelowe said:
This is also interesting, as Hyde claims he finds vasculitis in the brains of his patients (with little in the way of clinical studies to prove it, I must say).
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I don't think one should jump from the vaculitis that causes peripheral neuropathy to brain vasculitis. vasculitis is a rag-bag term that includes a lot of dissimilar processes. I would be very sceptical about claims of brain vasculitis in ME.

Acute involvement of brainstem in an infectious illness is likely to produce coma.
 
adambeyoncelowe said:
Mass hysteria does seem very unlikely, and I'm not sure we can reasonably assume every investigating medical team made exactly the same mistakes years and many thousands of miles apart, either, but I accept that there isn't any objective evidence of a localised lesion.
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I was not aware that 'mass hysteria' was considered to be a form of 'hysteria' in medical terms. I thought it was more a lay term. This is where I think it all gets very woolly. It is not clear to me that McE and B meant hysteria in the sense that Wessely would recognise, for instance. They say we all have a bit of hysteria from time to time. I guess that's psychiatrists for you.

And there is a sort of circularity to the idea that it is surprising that lots of medical teams made the same mistake I think. Let us say that perhaps 1000 times an initial case has appeared in a hospital with a fever and apparent neurological signs. In 980 of these the attending doctors have concluded that this is nothing very much and nothing more is said. In 20 the attending doctors raise the hare of polio or something similar. The word gets around rapidly, especially if the first case is a doctor and the next one a wad sister. The attending doctors start over interpreting like the patients, as Snow Leopard suggested. That could easily happen a few times. But we never here of the 980 times it didn't.

It may also be worth remembering that Ramsay was world famous as the author of a textbook on the classification and description of infectious diseases. Acheson was an infectious disease epidemiologist.
 
adambeyoncelowe said:
Was a polio panic present at each and every site?
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Acheson's comment is:

At the Royal Free Hospital, no patient with poliomyelitis had been admitted to the hospital prior to the outbreak, nor was the diagnosis entertained in the initial cases. There was no undue apprehension about poliomyelitis among the hospital staff, but rather about infectious mononucleosis which was the early diagnosis. In spite of this the course of the disease and type of neurological involvement was similar to that found in Los Angeles. in the Coventry outbreak six of the twelve patients had been nursing poliomyelitis cases for several years, and it is difficult to imagine why such experienced persons should suddenly manifest a hysterical reaction to the disease. In the Middlesex Hospital, Berlin and Bethesda cases there was no known poliomyelitis and, in the early cases at least, no reason for anxiety about it in the communities involved.

Edited to correct proofreading inadequacy. I keep wondering where words disappear to.
 
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Jonathan Edwards said:
I suspect a polio panic was present every time a patient came in to hospital with a fever and neurological symptoms in the 1930s-50s. Most other infections had become manageable by then but polio was still a concern to all parents in 1955. My wife was not allowed to swim in public baths because her father was a doctor and feared she would get polio. Infectious diseases were what worried people in those days, rather than slumps in the stock market.

I agree that it looks as if both Gulf War Illness and ME may involve some long term structural or physiological change to brain stem, basal ganglia or cortex. But that would not fit with ocular palsies, glove and stocking sensory symptoms or monoplegias.
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Thank you.
 
chrisb said:
Acheson's comment is:

At the Royal Free Hospital, no patient with poliomyelitis had been admitted to the hospital prior to the outbreak, nor was the diagnosis entertained in the initial cases. There was no undue apprehension about poliomyelitis among the hospital staff, but rather about infectious mononucleosis which was the early diagnosis. In spite of this the course of the disease and type of neurological involvement was similar to that found in Los Angeles. in the Coventry outbreak six of the twelve patients had been nursing poliomyelitis cases for several years, and it is difficult to imagine why such experienced persons should suddenly manifest a hysterical reaction to the disease. In the Middlesex Hospital, Berlin and Bethesda cases there was no known poliomyelitis and, in the early cases at least, no reason for anxiety about it in the communities involved.

Edited to correct proofreading inadequacy. I keep wondering where words disappear to.
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This is also why I have trouble believing McEvedy and Beard's arguments. They may have been right that the objective neurological evidence wasn't there, but I don't think that rules out a neurological pathology altogether, or that the kind of mass hysteria they claim happened instead.
 
chrisb said:
Acheson's comment is:

At the Royal Free Hospital, no patient with poliomyelitis had been admitted to the hospital prior to the outbreak, nor was the diagnosis entertained in the initial cases. There was no undue apprehension about poliomyelitis among the hospital staff, but rather about infectious mononucleosis which was the early diagnosis. In spite of this the course of the disease and type of neurological involvement was similar to that found in Los Angeles. in the Coventry outbreak six of the twelve patients had been nursing poliomyelitis cases for several years, and it is difficult to imagine why such experienced persons should suddenly manifest a hysterical reaction to the disease. In the Middlesex Hospital, Berlin and Bethesda cases there was no known poliomyelitis and, in the early cases at least, no reason for anxiety about it in the communities involved.
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I find that confused. Polio was relatively rare by 1955. Only one of my class mates was thought to have had it. But fear of polio was widespread. The absence of any recent cases at RFH is not relevant, I think. If infectious mononucleosis was first thought of it seems likely that there was an outbreak of a pretty severe febrile illness without any neurological features at first (EBV infection does not usually have neurological features). The type of neurological involvement was not like polio but what McE and B record looks like the sort of symptom pattern non-medical people might fear polio or something similar might be like. The last bit about people near the Middlesex having no reason to be anxious about polio is not right - that is where I lived and parents were always worried about polio.

At some point a patient may have had an overt nerve lesion. It would not be surprising if someone arrived with a facial nerve palsy for instance, since facial nerve palsies occur commonly anyway and possibly as a spin off of acute viral infection. Something similar might occur repeatedly from time to time all over the world and if other people got the febrile illness the occurrence of similar nerve-type symptoms, on the basis of suggestion and fear might well be similar.

The fact that people in Coventry had been nursing polio is not relevant. Presumably they caught a virus and were acutely unwell. It would be unsurprising if they suddenly panicked they might have something like polio, knowing what it could do, especially if someone else had been admitted with something like a facial palsy at the time. (I am not clear whether then other outbreaks had facial and ocular palsies or how similar things really were.)
 
adambeyoncelowe said:
This is also why I have trouble believing McEvedy and Beard's arguments. They may have been right that the objective neurological evidence wasn't there, but I don't think that rules out a neurological pathology altogether, or that the kind of mass hysteria they claim happened instead.
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I think McE and B give a pretty good case for ruling out neurological pathology for the symptoms they analysed. They tell us that all neurophysiological studies were normal - i.e. objective tests of nerves showed normal function. Acute febrile delirium is a sort of neuropathology but that does not merit a new name for an acute syndrome.

Somehow we have to make an inference about what was going on when a group of people reported what looked like neurological signs but objective tests showed nothing wrong with the nerves. That is a very common situation and I personally do not know what the mechanism is but it seems fair to say that it does not involve something wrong with those particular nerves.
 
Fascinating discussion. Thank you everyone.

In my often simplistic view of things I have reached this tentative line of reasoning:

No one can be sure now whether the Royal Free sufferers of what Ramsay defined as ME had an acute neurological infection, or a virus of some sort that seemed to cause some neurological looking symptoms and signs that weren't actually neurological in origin, and what was recorded in their notes does not match the signs of neurological illness.

Some of the sufferers from this outbreak went on to develop long term disability, and the name ME became attached to that long term condition, though it may have originally been intended as the name for the acute illness.

Ramsay continued to see these patients with long term illness and wrote a set of criteria to define the condition they now suffered from and attached the name ME to that.

So ME became, with Ramsay's definition, the long term condition with a particular pattern of symptoms.
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Others over the following years who developed the same or similar set of long term symptoms following other acute infections were also diagnosed with ME.

So ME became the name for any long term illness with a similar symptom pattern following a virus, though some still retained names like Chronic EBV or Post polio syndrome. New ones are arising following other infections like Ebola.

So it looks like the key thing in this condition or group or conditions is not the specific virus that triggered it, but some biological problem arising from the body's reaction to fighting an infection, but we don't yet know what that is.
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Meanwhile, McEvedy and Beard looked at the medical records from the Royal Free outbreak and published their conclusion that the Royal Free patients had not had a neurological condition, and that therefore their neurological symptoms were 'hysterical', meaning non neurological in origin. This was quite likely a correct analysis from the patient records.

However, the next step is not logical and is the step that has done so much harm. Their conclusion was widely publicised as meaning that the long term illness that some of Royal Free patients suffered following this acute infection was also 'hysterical'. A leap of logic that doesn't make sense but has done vast damage since it was picked up by other psychiatrists like Wessely who chose to apply it to all 'chronic fatigue' conditions including ME.
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In summary: Somehow the conclusion that one particular triggering infection was not neurological (hysteria) has turned into the conclusion that therefore nobody who gets a long term disabling condition following an infection is really sick (hysteria or conversion disorder). The lack of logic here beggars belief.

Is this an accurate (albeit oversimplified) version of events?
 
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Jonathan Edwards said:
The fact that people in Coventry had been nursing polio is not relevant. Presumably they caught a virus and were acutely unwell. It would be unsurprising if they suddenly panicked they might have something like polio, knowing what it could do, especially if someone else had been admitted with something like a facial palsy at the time.
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Is that sufficient evidence upon which to base a hypothesis? And what tests should one carry out to seek to refute it?
 
Trish said:
Fascinating discussion. Thank you everyone.

In my often simplistic view of things I have reached this tentative line of reasoning:
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Is this an accurate (albeit oversimplified) version of events?
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That is certainly how I see it. McE and B have done a huge amount of harm despite the fact that their conclusions on acute illnesses in outbreaks are irrelevant to the problem of ME as now defined.
 
chrisb said:
Is that sufficient evidence upon which to base a hypothesis? And what tests should one carry out to seek to refute it?
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I think it is sufficient to propose a slightly differently worded hypothesis from McE and B, namely that 'suggestibility' or other subjective factors altering symptom presentation was not ruled out by those analysing the outbreaks. McE and B wade in with 'hysteria' but their idea of hysteria seems to be more what people would call suggestibility - something that we are all liable to, without any need for invoking secondary gain etc. When you are seriously ill it is very easy to misread your own sensations. I've been there.

Refutation would involve doing neurophysiological testing to show that there were in fact nerve lesions. That was done at RFH and the hypothesis was definitely not refuted. It was corroborated by an absence of findings.
 
Jonathan Edwards said:
I think it is sufficient to propose a slightly differently worded hypothesis from McE and B, namely that 'suggestibility' or other subjective factors altering symptom presentation was not ruled out by those analysing the outbreaks.
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To try and narrow this down a little before considering it in detail, who is meant by "those analysing the outbreaks"? Clearly McE and B and Acheson. Gilliam (although that is only one outbreak), Ramsay, Jenkins probably. I don't recall whether Behan did in his 1988 paper. Wessely presumably, but as I am not at all sure that he can have read Jenkins or Acheson, he can probably be discounted. Hyde.

I suspect that a problem may arise in that such a concept was never ruled in and therefore not positively ruled out.

It was interesting to note that in his report on the Dalston outbreak Wallis reported that he was told by district nurses that similar cases were occurring in neighbouring practices, and the helpful consultant psychiatrist reported other cases having been referred to him. It is hard to see how suggestibility could have played a part in such cases, although, of course, they are not recorded.

Edit spelling of Acheson
 
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chrisb said:
I suspect that a problem may arise in that such a concept was never ruled in and therefore not positively ruled out.
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By 'those analysing' I was really referring to those that McE and B refer to as dismissing hysteria. And McE and B quote an active dismissal, not just a never ruling on.

I wouldn't put too much weight on district nurses saying they had seen cases too. In medicine one is bombarded with cases of all sorts all the time. It is very easy when in a conversation about a pattern of illness to recollect something similar in one's own experience. If district nurses had encountered people with significant neurological illness they would have been sent to hospital. And, as I have mentioned, the sorts of symptom patterns McE and B analyse are probably referred to psychiatrists every week, having been considered as not true nerve lesions.
 
Are we sure that "suggestibility" is not merely a particular form of "hysteria" in cases where groups are affected?

I have this from Jenkins:

c) Mass hysteria involves the epidemic spread of hysterical symptoms and is usually due to the combined effects of suggestion and shared apprehension which may occur amongst adolescents and young adults who are in close proximity.

Rachel Jenkins. Post viral fatigue syndrome (Myalgic encephalomyelitis) eds Jenkins and Mowbray Introduction p29 Sub heading Hysteria and ME.

Does the idea of suggestibility in adults along, with shared apprehension, take us any further away from the concept of mass hysteria-whatever that may be? Or does it take us sufficiently far away to be regarded as a separate concept.
 
chrisb said:
Are we sure that "suggestibility" is not merely a particular form of "hysteria" in cases where groups are affected?
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When I used it I was not implying hysteria. If hysteria implies secondary gain and conversion then definitely not. Jenkins's account is problematic because it talks of spread of 'hysterical symptoms'. Does that mean symptoms due to hysteria or the sort of symptoms that one also sees in hysteria or what? And what does Jenkins think hysteria means?

To me it is all irrelevant in the end because it is about an acute illness that is not the ME we are interested in.
 
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