Is it worth explaining the difference between ME and CFS to the public??

[Bob]

Bob, I'm not really seeing any real difference in what Ramsey says to what has been said in this thread. I have read all of his info and it is still how I have described it in this thread. As I said historic M.E. does not mention "chronic fatigue" which is different to post exertional fatigue. The updated definitions included chronic fatigue, that is one of the symptoms that has led to it becoming a "catch all" name for anything with fatigue in it.

I was told that I would be better in 2-5yrs and to rest, which is what I did. Nearly 20yrs later i'm still sick. What I have wanted to know is did he follow up the one's that made a "full recovery"? were they still well 10 yrs later?, did they really have M.E.. I have never met someone with real M.E. that has recovered, gone into remission and led an almost normal life for years at a time, yes. Most doctors will tell you the same thing. Is it possible that is what happened to those patients? Remission, not recovery. I really do wonder..

But it still comes down to recovery or remission, remissions of 10 years are not unheard of.

I should say my personal view that it is lifelong has only been developed in the last few years and relates to observing the history of the last 16 yrs of this disease, and the changing view amongst M.E. specialists. It is not related to historical literature. Most M.E. specialists now agree that "recovery" is rare. But that does not mean your health can't improve to the point of being able to be almost normal, it just means you will always have the disease.

Please note that my comments were not aimed at anyone specifically... I am commenting on the thread in general.

The impression given on this thread was that fatigue is not a predominant feature of historic ME. The Ramsay literature totally contradicts that.

It was also said that the historic literature says that 'ME' is a life-long condition, giving the impression that ME is always a lifelong condition.
I don't know what the actual figures on remission are for ME, but as we are discussing historic descriptions of ME, then for factual accuracy we should also be mentioning the fact that Ramsay says that it is not always life-long, otherwise we are misrepresenting the facts. The most up-to-date work on ME may have a more detailed analysis of this specific issue.

Tuliip, the discussions on this thread have been about the factual historic descriptions of ME, and while I value your personal views, I think we should be careful about confusing your personal views, expressed above, with the factual literature.

 

[Bob]

Hi Bob,



From what I can discern, post 1988 and into the 1990s, that would have been the picture created in the literature, with confusing references and use of terminology causally being employed by researchers.

Exploring this aspect of the history, has been a real eye opener to me. I can see the damage and confusion that this alone has done, which is often not acknowledged. Really though, if you take some time to read through the literature and see the mish mash of terms used - you simply shake your head and say - as was said somewhere else in this thread - what a mess!

But why? Was it a struggle to meet new paradigms that appeared similar but were not the same and that gave rise to confusion? Was it politics? Was it funding based/grants driven ? Was it simply a reflection of the researchers writing and work style? Perhaps it was a combination of all of these.

I always viewed science as being meticulous for detail, but I dont hold this view anymore and realise that attention to detail must come from the research scientist engaged in a study and unfortunately, this is not a trait common to all individuals and it is not desired by those who do not have it. Those that do not have it, tend to see those who value it, as pedantic, nit picking, wasting precious time and failing to see the big picture. Hence some researchers personal work styles that favoured a broad brush/big picture approach may not have necessarily placed value on the need to understand and or applying the correct terms or look closely at what appeared, for all intents and purposes to them - as something that was the same.

Was this a wonderful example of the failure of peer review and if so, why? Or was it simply a failure to appreciate any significance to the matter -and or have any real foresight in what would eventuate? I dont know, but it is something I have from time to time, looked into and tried to work through.

With regard to historical ME, the general body of literature points to primary ME as being associated with enteroviral infection .

A lot of the literature that ME is based on, is based on documenting patient symptoms that arose out of the many historical epidemics.



EPIDEMICS

In the good old days, when ME was acknowledged and the relationship between it polio was better understood and known, enteroviral infection in a patient would be tested for quite quickly - especially in the context of an infectious outbreak. The infectious period for enteroviruses is around 3-7 days. In such circumstances, evidence (via serology/stool analysis) would usually return a positive result - because the tests were run close to the infectious period and viral loads in the blood (stools) were relatively high.

The further away from the date of onset though, the more difficult it becomes to get such.

Sporadic cases though are different.

With epidemics or outbreaks, doctors are eventually alerted to a possible ME diagnosis and are more likely to consider and test for it, simply because it is on their radar via larger numbers of patients presenting with symptoms and or infectious diseases bulletins put out by NIH etc

However today, at least here in Australia - reporting and monitoring of infectious diseases within the community has changed a good deal, to the degree that outbreaks are not reported and monitored as they once were and I believe quite a few that would otherwise be reported to doctors, are not now and so, fly under the radar. Unless there is a large outbreak or one within a small community - doctors are unlikely to spot it and report it either. So there is no feedback loop for the wider medical community to alert them to the possibility of these viruses circulating - in order to consider them within their patients. I wonder the degree to which epidemics of ME are circulating within the community and going unmonitored for these reasons)




SPORADIC / NON EPIDEMIC CASES


So, in an epidemic a potential diagnosis is on a GPs radar, when a patient walks in with similar symptoms. Without this, it makes it harder for a doctor to be able to distinguish a potential case of ME from other l gastro intestinal/general respiratory like bugs and they dont generally run blood or stool tests for that today, as we know because of NIH monitoring how many tests doctors are ordering etc. It was different in the days of polio and when ME both had a larger profile, I am sure - which would have justified doctors undertaking such tests.

So the patient leaves and the initial illness passes and then they have a whole new range of symptoms (which they dont associate with the triggering illness) and by the time they return to a doctors with these strange new symptoms, it is usually well past the time frame for a test that would produce a positive enteroviral result. Further, doctors these days do not make the association between that earlier onset illness, and the subsequent symptoms that follow with ME. Sometimes, the patient does not report the triggering short gastro intestinal or respiratory like illness associated with enteroviral infections in ME either, because they dont think its relevant. Doctors pressed for time and not knowledgeable on ME - dont think to ask. This is one of the problems - not only in diagnosing sporadic cases - but in gathering a body of evidence further supporting the enteroviral ME connection in such cases, that might otherwise be reported in medical literature today -that would provide stronger evidence for enteroviral ME in sporadic cases.

I would suggest that this is another reason why Hyde goes for evidence of CNS damage via the CNS tests he recommends. If you cant get evidence of CNS damage (which enteroviruses associated with ME are known for) then in a sporadic case (and today most of them will be, I believe for the lack of surveillance measures I alluded to) this way, you overcome the problem associated with serology based evidence that diminishes with the flux of time. Of course, tissue biopsy of the stomach, performed by Dr Chia and Prof KDM - is now available and is a new method of gathering evidence of enteroviral association, to assist in diagnosing ME in sporadic cases - in support of other symptoms and other evidence (ie CNS damage) of ME.

However, Dr Chia's technique is a recent one and that is why (I believe) Hyde relied heavily on other tests to show damage to the CNS - which is consistent with enteroviral infections.

Before Dr Chia's technique, Hyde did not place a lot of reliance in serology/stool tests for picking up enteroviral infection in his patients, because of the acknowledged limitations with serology/stool tests which were not done contemporaneous to or soon after the onset. (This was also one of the reasons that caused Dr Chia to develop his techniques and studies for enteroviral tissue biopsy)

Further, there was (prior to Dr Chia's research and work) a view in the literature (that had met small challenges in the past) that entroviral infections did not hang around in the body for years, but were in fact, short lived infections. It was reasoned that gastric acid in the stomach would make it an unhospitable place for enteroviruses to survive for too long after infection. Mowbray (UK) questioned and successfully challenged that assumption, as did a study of Dowsett and Ramsay (UK). Dr Chia's work confirmed these earlier findings but that these infections can and do last in patients for years.(He also developed a technique for finding the virus from a certain area in the gut and testing the tissue)

But prior to such work, the assumption represented a challenge to enteroviral association in ME and its role in contributing to long term disability. (John Chia's research shows that viral load in tissue equates directly to the level of disability in patients).

Prior to the work of Chia in recent times, Hyde maintained, acknowledged and upheld the general body of scientific evidence supporting enteroviral infection as the cause of ME and its association to prolonged illness in patients, because of the vast body of scientific evidence collected from over 64 historic epidemics within which patients were studied.

But with sporadic cases and the lack of tools that could consistently and reliably pin point enteroviral infections in patients, well past infectious onset, I believe Hyde although states that it is a cause in such cases (and he has found it in patients after infectious onset) generally exercised a more cautious manner - rather than being so assertive on the point as it related to sporadic cases.

Of course I believe he also did so - because of the introduction of CFS and his findings that most cases of CFS are in fact cases of missed diagnoses.

In his cautious exercise and demand for evidence in sporadic cases of CNS damage, Hyde in the past, has also acknowledged that there have been some odd cases of ME, where significant exposure to toxic chemicals and vaccines have appeared to play a role. From what I have read, I believe he sees these cases as being difficult to explain -as they lie outside the general body of what is known and accepted and I believe (prior to Chia's technique and or better serology/stool analysis tools for enteroviral detection) of what he saw,at the time, as limited tools to assist in identify enteroviral infection .

Today we know, enteroviral infections do persist and can be isolated in the tissues of the stomach in ME patients. It is an invasive procedure and not ideal I agree, but we have that. Studies of patients using this technique might be useful however, to push research to develop further research in this area, for better serology or other less invasive tests.

I dont know whether Hyde in light of the techniques used by Chia and Prof KDM today, would insist that the odd ME cases (or atypical ME cases) he has witnessed associated with toxic chemical exposure and certain vaccines, undergo tissue biopsy though in order to establish an enteroviral connection. All the same, the impression I am given from my reading of these cases, that he has mentioned briefly suggests to me that Hyde views these cases as atypical.

It would be very interesting to know though, whether these atypical cases also present with enteroviral infection and whether the toxic elements they were exposed to, provoked a viral response of an underlying or pre-existing enteroviral infection.

Anyhow, that is my take and analysis on the matter. Others here with knowledge on historic ME might have another view and understanding, and if so, it might be interesting to hear from them too.

At the end of the day, from my reading, the literature does make a good case for primary ME being caused by enteroviral infection - as evidenced by a large body of literature produced from studying patients in historical epidemics.

Thanks insearchof, that's a really interesting post.

This puts John Chia's work in a new light for me... I wasn't aware of the relevance of his work because I wasn't aware of the significance of enteroviruses in relation to the historic definitions of ME.

So I'm going to have another look at Chia's work, with a renewed interest.
It will be interesting to see what percentage of Chia's patients are testing positive for enterovirus.

I hope that was useful in answering how ''clear cut'' or otherwise, the enteroviral association with Historic ME is.

Yes, thanks very much, it was helpful... But I'm still not sure about it after reading the Ramsay literature... I'll keep reading.

I'm going to read through some of the Hummingbird literature next.


Note: Please keep in mind that I'm now slowly catching up with reading through this thread, so my all of comments are not informed by the latest posts.

 

[insearchof]

Hi Bob

I agree... This is a work in progress for me, and those were my initial observations based on the Ramsay literature (3 of Ramsay's papers)...

I've got much more reading to do...

I'm slowly working through it all, and will start looking at the Hummingbird literature next.

I'll read through all the responses to my posts as soon as I can. But it will be slowly.

I have not looked at the HFME literature for a little while, so it will be good to reconsider it here.

 

[Boule de feu]

I don't understand why fatigue could not be part of the equation. If we have a look at the different symptoms, many of them cause fatigue.

Chronic pain causes fatigue. The more pain you have, the more fatigue you get.
The more fatigue you get, the more pain you have.

Muscle fatigue, myalgia, headache, vertigo, chills, spasms, etc.

My body is always compensating for the vertigo and for the orthostatic intolerance.

I do suffer from all, but the ones that are giving me the biggest fatigue is "reversal of sleep rhythms" and bouts of severe inflammation. The chills and the low-grade fever do tire my body.

I can't sleep at night. I can't sleep during the day.
This in itself causes fatigue.

The fatigue I experience is exhaustion. It is at a cellular level.
It's PURE exhaustion. Can't move. My gait is so slow now. I think a turtle could easily pass me on the street.

I'm not sure if it is the case for everyone, but when I got sick in 2005, I could have slept 15 to 20 hours a day.
Now, if I get 3 or 4 hours, I'm very lucky.

When I watch videos of severe ME sufferers on TV/YOU TUBE, they are lying there.
I feel so sorry for them!
They can't move. They can't be in the light. They can't make the effort to eat.
We must feed them or intubate them.
They can't have a conversation. Isn't this fatigue?

Maybe we don't define fatigue the same way?
Are there several definitions?

Personally, muscular fatigue is fatigue at it's finest. It's the hallmark fatigue.
But again, maybe I don't define it properly.

 

[Bob]

Hi Bob

The Dowsett Ramsay paper published in 1990 is an interesting paper.

I see you have also referred to little bits of the paper that you have found personally interesting, which I agree with you they are. But context is important both with respect to how those little bits of information sit within the overall document, its focus and intent - as well as a more extensive body of work.

Yes, I did pick out excerpts that particularly interested me, and that are relevent for this discussion, but I tried to pick out a balanced and fair representation of the information in the papers.

The opening paragraph of that study makes it clear, that purpose of this study was two fold:


(a) one to demonstrate the association bewteeen ME and enteroviral infection and

(b) two that unique clinical and epidemiological patterns associated with enteroviral infection distinguish ME from PVF states.

Yes, but "patterns associated with enteroviral infection" is not the same as having an "enteroviral infection."

Ramsay says: "This must not be taken to imply that Cocksackie viruses are the sole agents of myalgic encephalomyelitis since any generalised virus infection may be followed by a period of post-viral debility. Indeed, the particular invading microbial agent is probably not the most important factor. Recent work suggests that the key to the problem is likely to be found in the abnormal immunological response of the patient to the organism."

So Ramsay's focus on enteroviruses, does not seem to match up with your own.
I've yet to read Hyde's work, so I accept that I don't have the full picture yet.

"One of the first points made is that results show acute or sudden onset in 81% of patients."

So does this mean that 19% of patients do not show 'acute or sudden onset'? If so, then this is another contradiction to what has been said on this thread. It has been said on this thread that historical ME can only be sudden onset.

I would also suggest to you Bob, that 100% muscle fatigue (a very specific type) found in the cohort, although high, is not surprising because it was specifically selected for amongst the cohort in the studies design.

That's not a correct suggestion... Ramsay consistently refers to fatigue being the predominant feature, in all of his 3 papers that I've read. That is stated without any ambiguity in each of his papers.

Bob, no one has suggested that enteroviral infection must be found 100% of the time.

I know that you have kindly taken time to explain carefully the details about enterovirus infection, and clearly stated that enterovirus is not found in all cases.

But the way some posts have been written, they gave the impression that ME is caused by enteroviral infection in 100% of cases.
I accept that ME might yet be proven to be caused by enteroviruses in 100% of cases, but this is not the case at present.
People appeared to be implying that this is a fact, even if they didn't actually say that.

But the fact is that enteroviral infection, according to Ramsay, is an association with ME, and no more than that.
I'm not trying to deny an enterovirus association... I find it very interesting... But I am trying to present the facts, as I read them, accurately.

 

[Bob]

I think you have made a couple of mistakes in your analysis and interpretation of the Ramsay Dowsett paper. I need to address the other Ramsay paper you posted though.

I think it is a little unwise to base your conclusions on two papers - one of which you appear to have taken out of context or viewed through a distorted lens - and then suggest that what has been posted in this thread by others is at direct odds with Historic ME. It is not and in fact, I would hope that my post on the Dowsett and Ramsay paper shows quite the contrary to be true.

Hi insearchof,

I may well have made mistakes, and I'm happy to be corrected if that is the case.
I did make it clear that these are my initial impressions, based on reading Ramsay, so I view this as a fluid process of learning, and am happy to change my interpretations as I explore further.

In terms of the paper that you say I have taken out of context and viewed through a distorted lens, I don't think that I agree with this.
I read your earlier post, and I accept that one of Ramsay's papers was related to specific research on a specific cohort of patients, but I did not try to present this as anything other than that. Ramsay was clearly expressing his views about 'ME' in that research paper, based on his entire knowledge of the disease, as it affects all patients. I know that the list of symptoms, and the enterovirus detection rates were only related to that specific study, but the results were still very interesting, and relevent.

I still maintain that much of what has been said or implied on this thread (but not everything) contradicts what Ramsay has said in three of his papers. I have quoted three of Ramsay's papers in total. Two from 1986, and one from 1990.
I am only quoting Ramsay. I'm not pretending that Ramsay's 3 papers are giving me a full picture. But he is an authoritative source for historic ME.

I'm not going to make any solid conclusions until I've studies more up-to-date research from Byron Hyde and others.

 

[Bob]

Hi Bob,

This article was written in 1986 when there was much confusion between the terms ME and PVFS and the article needs to be acknowledged in that context. We looked at this earlier in the thread. Please see post #90 here
http://forums.phoenixrising.me/show...erence-between-ME-and-CFS-to-the-public/page9

Without uinderstanding the historical context and historical sequence of events that impacted on historical ME literature and promoting only two papers, it is easy to see ME narrowly and through a distorted lens - which might make it appear as though, there is no difference between ME and CCC and or that ME PVFS and CCC are all the same, when they are not. Again the ICDs attest to this.

I accept everything that you say here...
But Ramsay is often quoted as being one of the most authoritative sources on ME.
So I had assumed that what he had to say in 1986 had not been contradicted in more up-to-date research, but had just been built upon.
I will stop assuming that, and I'll carry on reading.

 

[insearchof]

Hi Bob,

Given that you are still playing catch up and have not read my posts, you might like to do so and then reconsider what you have posted here, as this statement of yous is, I believe incorrect:

The impression given on this thread was that fatigue is not a predominant feature of historic ME. The Ramsay literature totally contradicts that.

I know your still playing catch up on reading my posts, but when you do so - you will see that the statement you made here is not correct.



As for the impression given on this thread, that ME is always a life long condition I have addressed that also in my previous posts which I am sure you will get to.

Ramsay in that *one article *circa 1986*suggests-* that it might not always be life long. Agreed.

There is support in the literature that some people if given complete rest during the acute phase of the illness (first couple of months after illness onset) can and have recovered.

How much support for that in the literature I dont know - I would have to sit down and do an analysis on this.

However, the second part to that is this.

The literature and even Ramsays own subsequent research findings in 1990 which you cite (Dowsett and Ramsay1990) calls into question the idea of ''complete recovery'', as well as raising the question of what ''recovery'' might be regarded as for the purposes of ME - a condition known in part, for ''remission's'(of various durations) and relapses (also of various durations). So keep that in mind.

There is some suggestion (as I said, how much would require me to sit down and look at it carefully) in the literature that if ''recovery'' does occur at all- then it may be in the acute phase (shortly after illness onset with complete rest).

However, I believe that this represents the exception and not the rule.

"'Complete rest'' at illness onset today is rare though and being rendered unconscious (like the three patients he refers to as recovered) or put into an induced coma is unlikely to occur.

In the good old days, irca 1934 -when medicine recognised the value of bed rest for most ill patients, this might explain why there were indeed reported cases of recovery during the acute phase of the illness. It is less likely today I would suggest, and for the problems I have suggested (re failure to detect outbreaks, the delays in conducting enteroviral testing after illness onset and limitations with those tests).

But Dowsett and Ramsay both did and Dowsett continued to emphasize- the importance of complete rest - especially during the early stages of the illness.

One example from the historic ME literature

Dr Albert Marinacci, was a doctor at the LA County General Hospital at the time of not only the well known 1934 ME outbreak there, but also subsequent ones. He went on to write a book in which he described the features of ME and in a subsequent interview on this matter with Dr Karl Von Hagen, reported that patients from the 1934 outbreak seen 50 years later, had not recovered. Those that he followed for a long time, were disabled and very few made a complete recover.

In addition to treating and following epidemic cases, both Marinacci and Von Hagen saw a number of sporadic (non 1934 epidemic(s)) ME cases and they followed these cases for 16 years.

They report that the findings in those patients (who progressed to the chronic phase of the illness) and who were chronically affected, were consistent with those seen in the epidemics.

In this group they did note though, some recovery of patients in the acute phase (just after illness onset 3-6 months). In the next phase the chronic phase they said that patients could have the illness for years with periods of improvement for short durations as in the 1934 epidemics.

So findings re recovery - if and when -were consistent in both epidemic and sporadic groups.

However, from my reading it seems to me that those that recover just after illness onset in the acute phase -seem to represent the exception than the rule.

These reports though, are consistent with what is known about the nature of enteroviral infections generally.

Studies have shown that there is an association between hormones (progesterone and cortisone in particular) and certain strains of coxsackie enteroviral activity. A study Gatmaitan et al showed for instance, that a certain strain of the coxsackie virus stimulated by hormones produced by activity induced stress, increases viral load of coxsackie B3, 530 fold in mice.

So complete rest at illness onset, may assist in seeing the recovery of some people in the very early stages of illness. That though is subject to the caveat that this will also be dependant on viral strain, virulence, age and individual susceptibility and their immune health.

However, enteroviruses are also known as presenting long term infections in ME patients who progress to the chronic phase (which I would say is the general rule rather than the exception). Ramsay and Dowsetts study showed persistent enteroviral infection in their study co hort of 402 patients by finding evidence of coxsackie enteroviral infection in persons who had ME for many years. Chia and Mowbray et al have also shown this.

As enteroviruses go to the tissues and hide there, they behave in a fashion similar to the hidden repositories reported in HIV patients (hidden repositories associated with latent infections) and proliferate under certain circumstances. Hence the remission and relapsing nature of the illness. Consider here, what I also said previously on the finding of the Gatmaitan study with hormones, and activity.

The findings of Ramsays study in 1990 show that 69% of patients in their co hort who had reported having the illness over a collective period of 60 years, were not improving and 25% had never experienced a remission or worse.

What happened to the other 31% reporting improvements is not known. Did this continue? How many did so or did not?

Even though this does not relate to historic ME, in the Hanson Bell XMRV study they also questioned what recovery meant in the context of CFS, with patients reports of recovery, not meeting generally accepted objective medical standards of such. It was suggested that those patients in that study that reported recovery, had not. It was thought that the patients reported such, because compared to where they had been previously (in terms of disability) the improvement felt like a recovery.

So to summarize -a small group of ME patients might recover on complete rest, within a short time after illness onset - though opportunities for this today are rare, I would suggest. Further, most of those seen as ME patients today, I would suggest are not those that recover but, are those that reach the chronic stages and in such patients the literature suggests that complete recovery is not the norm.

I will leave it there for now.

 

[Bob]

Hi Bob




Prognosis and Recovery

In the paper you cite, Ramsay states that he does not believe the illness is progressive - at least not in the way that MS is. That is not to say that it is not otherwise progressive, but I wil come back to this point.

He does that as the illness is not progressive in the same way MS is, then prognosis should herefore be relatively good.

I note, he does not say it is. He is careful there, and he also uses the term ''relatively'' good. That is important, because other literature highlight that ''recovery' as understood in ME is not the same as generally understood in other illnesses.


Further, prognosis is subject to and largely dependent on, the management of the patient in the early stages of the illness. Those who are given complete rest from the onset ''do well''. I note he does not say ''completely recover''.

He observes that the three patients that he does state did 'recovered completely'' were unconscious This however is not a common state in ME and most patients advised to rest, are not and are not placed, into an induced coma.

Also, we do not know what follow up over the long term, indicated in these three patients. So whether they did completely recover is questionable also, based on the basis of other ME literature - which questions complete recovery and that it may be more appropriate to say ''remission''.


Other literature would suggest that some do *appear* to recover, but these individuals usually fall subject to a relapse - sometimes years later. That of course is consistent with the notion of enteroviral infection that is left untreated and which exists in the tissues long terem (Chia).

Marinacci et al who treated a lot of patients out of epidemic oeriods said that most of those patients never recovered and were ill 40 years after the illness onset.

So complete recovery is questioned elsewhere, even by Ramsay himself in his own subsequent study you previously quoted (Dowsett and Ramsay) showed that over 50% of patients did not do so and have a cycle of remissions and relapses. 25% of this group never experienced a remission period at all.

Ramsay did not state that all patients recovered. Just that recovery was possible in ME.

Ramsay clearly believed that a full recovery was possible, as he stated, but not in all patients.
He may have been mistaken about ME patients making a full recovery. I don't know. I am just reviewing the literature.

Progressive

It is hard to know what he meant here. Progression in MS represents an escalation in symptom severity as it was explained to me. There is fluctuation in symptoms, together with severity. To say anything more, I would need to go back to some papers. So I will leave it there. Someone else might be able to elaborate in the interim.

In terms of what he meant by 'progressive', he describes this himself in his descriptions of the chronic cases of ME, quoted in this post:
http://phoenixrising.me/forums/show...-to-the-public&p=176624&viewfull=1#post176624

ME does not have to be caused or precipitated only by enteroviruses.


I refer again, to previous posts (in particular post #90). I dont think that there is general support for this proposition in the general body of historic literature on the matter. It is also why there ME and PVFS are both listed at G93.3 ICDs It being recognised that a particular virus has been associated and found to cause CNS damage in patients diagnosed with ME and other viruses as the cause of PVFS.

As previously stated though, Hyde does refer to this odd group (vaccine and toxic chemical exposures) in ME which I referred to as atypical ME. However these were cases, which lie outside of what is known and accepted as the norm by the historical ME literature. The limitations with serology/stool analysis for enteroviral detection were unable to assist here obviously. It would be interesting to see whether they had such via a tissue stomach biopsy - in accordance with the method used by Dr Chia.

OK, thanks, I'm going to look into the more recent literature about ME and enteroviruses.

The dominant feature of ME is fatigue.

There is no support for this, either on the basis of the Ramsay literature you quote Bob - and especially when you place them within an historical and wider context of the general body of historic ME literature.

Fatigue is a symptom common to many illnesses. I would even go as far as saying that it is not regarded as a dominant feature in any illness outside of CFS and even then, it is an unremitting fatigue.

Ramsay absolutely, consistently and categorically states that fatigue is the predominant feature in ME. He states this in the three different papers that I quoted from.
Nothing has been misquoted, presented out of context, or distorted, in terms of his quotes about fatigue.
Indeed, he says fatigue is one of the only features that is present in 100% of his patients, apart from a very few isolated individuals who had all the other features of ME but without fatigue. This, he suggests, was because they were in a state of remission.

Here's a quote, again, from a 1986 paper:

"The Myalgic Encephalomyelitis Syndrome"
A. Melvin Ramsay M.A. M.D.

The unique form of muscle fatiguability described above is virtually a sheet-anchor in the diagnosis of Myalgic Encephalomyelitis and without it a diagnosis should not be made.

http://phoenixrising.me/forums/show...-to-the-public&p=176623&viewfull=1#post176623

You can't get much more categorical than that.

Here's a longer quote from the same paper:

Once the syndrome is fully established the patient presents a multiplicity of symptoms but these can conveniently be discussed under three headings, namely:

1. Muscle Phenomena

The unique form of muscle fatiguability described above is virtually a sheet-anchor in the diagnosis of Myalgic Encephalomyelitis and without it a diagnosis should not be made. I am informed of two families who are said to have all the conditions conforming to the clinical picture but lacking the muscle fatiguability. These cases should be very carefully reviewed. It is quite common to find that muscle power is normal during a remission and in such cases tests for muscle power should be repeated after exercise.

http://www.hfme.org/wramsay.htm

Thanks for the productive discussion insearchof. I'll keep reading.

 

[floydguy]

Again I believe there is a difference between muscle fatiguability and the fatigue described by the CDC definition. The CDC version of fatigue is more of an exhaustion and Ramsay's is more of a muscle weakness. I see that as a large difference.

 

[Bob]

Given that you are still playing catch up and have not read my posts, you might like to do so and then reconsider what you have posted here, as this statement of yous is, I believe incorrect:

The impression given on this thread was that fatigue is not a predominant feature of historic ME. The Ramsay literature totally contradicts that.

I know your still playing catch up on reading my posts, but when you do so - you will see that the statement you made here is not correct.

I have caught up now, and my statement was entirely correct, as outlined in my previous post. It is your statements that do not coincide with any of the Ramsay literature that I have read from 1986 or 1990.

The literature and even Ramsays own subsequent research findings in 1990 which you cite (Dowsett and Ramsay1990) calls into question the idea of ''complete recovery'', as well as raising the question of what ''recovery'' might be regarded as for the purposes of ME - a condition known in part, for ''remission's'(of various durations) and relapses (also of various durations). So keep that in mind.

There is some suggestion (as I said, how much would require me to sit down and look at it carefully) in the literature that if ''recovery'' does occur at all- then it may be in the acute phase (shortly after illness onset with complete rest).

However, I believe that this represents the exception and not the rule.

You might be right about this, but this isn't how the info was presented earlier in this thread.

"Calling into question" whether people recover or not, is not the same as saying that people with ME do not recover.



Some of the facts have been misrepresented in this thread, at least as far as the facts relate to Ramsay, who is considered an authoritative source.

I accept that I now need to look at the latest research in order to assess how the 'facts' presented on this thread match up to the latest knowledge about ME.

Thank you again insearchof, for this productive discussion.

 

[insearchof]

Hi Bob

Yes, but "patterns associated with enteroviral infection" is not the same as having an "enteroviral infection."

I am sorry but I am uncertain of the point your making here. The study showed very good evidence of enteroviral infection in over 50% of the cohort, if I recall and for reasons previously expressed, this was a very good result.

Ramsay says: "This must not be taken to imply that Cocksackie viruses are the sole agents of myalgic encephalomyelitis since any generalised virus infection may be followed by a period of post-viral debility. Indeed, the particular invading microbial agent is probably not the most important factor. Recent work suggests that the key to the problem is likely to be found in the abnormal immunological response of the patient to the organism."

So Ramsay's focus on enteroviruses, does not seem to match up with your own.
I've yet to read Hyde's work, so I accept that I don't have the full picture yet.

Perhaps your still playing catch up here, and have yet to read my post at #90?

So does this mean that 19% of patients do not show 'acute or sudden onset'? If so, then this is another contradiction to what has been said on this thread. It has been said on this thread that historical ME can only be sudden onset.

This is one study Bob. Are you suggesting that 81% showing sudden onset is not supportive of the general position (recognised elsewhere in historic medical literature) that the disease is understood as commonly having acute onset presentation?



How often do you see a study where they get 100% findings and outcomes?

81% is very high, and as such (together with other historical evidence that supports such - found primarily in the context of epidemics, I beleive) it is accepted as the general rule.


To explain the reason why 19% did not have sudden onset, maybe due to a pre existing illness unrelated to the enteroviral infection which made the 19% susceptible to the triggering enteroviral illness with which came subsequently sudden symptom onset associated with ME. This is not uncommon. I think I have referred to this elsewhere in the thread - and recently to Sandgropper. Perhaps this was not picked up in the patient history? But 19% is, in any event negligible and not sufficent to challenge the well established general rule supported in a vast body of literature.

Dr Chia for example, when taking a patient history carefully looks at this sort of thing and questions the patient very carefully.

He has noted that some patients cannot distinguish between an earlier illness and the subsequent illness onset (gastro intestinal / respiratory in nature) with the sudden and very clear cut ME type symptoms that follow. If you simply ask a patient when their health went down hill, they might report an initial unrelated episode (that would set them up for the enteroviral one) and sometimes the subsequent enteroviral triggering illness might be very mild - so in some cases it might be hard for the patient to even note the subsequent ME triggering enteroviral illness. Also, patients - by the time they get to an ME specialist, which can be years later - might have trouble remembering a mild enteroviral illness. But the give away is, as I understand it- the distinctive and sudden symptom onset, even after a mild infection.

'But there are also gradual onset patients who's symptoms and illness presentation does not fit what is known about ME at all. The historic literature (a lot of which relates to epidemics where these matters were clearly noted) report and support, sudden onset of symptoms as the general rule as witnessed in over 64 epidemics and with what is generally known about enteroviral related illnesses.


I view the study is a strong finding for the proposition stated for acute onset infection in ME and in support of the general rule. Again, it is one study. There is a lot more literature - in support of this in both epidemic and sporadic cases.

As for the assertion that it is always or can only be acute onset......
I dont believe that statement to be contradictory to the over all evidence (body of collective historical ME literature) which I understood the statement to be reflective of.

But perhaps you can ask for clarification from the person who made it.


This study finding (one document in the vast sea of historic literature) with an 81% result in this shows and supports the general rule.


General rules supported by repeated evidence (as shown in the literature related to epidemics in particular) are used to define illness, like ME. Physicans also use them for the purposes of diagnosis, in help them navigate their way through a sea of competing similar illnesses.

The stament made I see as representative of the general rule.

General rules in medicine which are well supported (ie 81% findings) are not usually qualified.

That's not a correct suggestion... Ramsay consistently refers to fatigue being the predominant feature, in all of his 3 papers that I've read. That is stated without any ambiguity in each of his papers.

I am sorry Bob, I disagree strongly with this and for reasons already pointed out in my previous posts. When you take something out of context - be a paragraph to highlight a point, or *one* document- out of its known historical understanding, then it will, as here *appear to be making the case you suggest. Again I refer you to my post #90.

I understand though, it is hard to see this when you are only setting out to read the vast body of literature collected over 50 years.

I said this:

Bob, no one has suggested that enteroviral infection must be found 100% of the time

Bob said in reply:

I know that you have kindly taken time to explain carefully the details about enterovirus infection, and clearly stated that enterovirus is not found in all cases.

But the way some posts have been written, they gave the impression that ME is caused by enteroviral infection in 100% of cases.

I accept that ME might yet be proven to be caused by enteroviruses in 100% of cases, but this is not the case at present

.

Sorry Bob, I should have said that it is not possible to find enteroviral infections 100% of the time, for reasons already stated. Not that they are not always associated with ME, because the literature points to the fact that they are - especially the literature detailing over 64 epidemics which makes the case strongly. From that literature comes a general and strong body of evidence from which general rules are formed. There are always the odd exception, but they are not usually a focal point in medicine- the general rule is.

Today (with Chia's stomach biopsy test) we should theoretically be in a position to show enteroviral presence in an ME co hort without the difficulties of the past associated with serology and stool analysis. Of Chias patient base, I recall reading somewhere that he spoke of 80% of his patient base as enteroviral postive ME and the remainder have other viruses and causes which he refers to as he CFS patients.

People appeared to be implying that this is a fact, even if they didn't actually say that.

I think people are doing their best Bob, within the limits of time and health.

I hope this makes sense and is not too repetitive. Its late here and I need to rest.

I will come back to reply to your other posts soon.

 

[Bob]

This is one study Bob. Are you suggesting that 81% showing sudden onset is not supportive of the general position (recognised elsewhere in historic medical literature) that the disease is understood as commonly having acute onset presentation?

No. I'm saying that it doesn't match up to what appeared to be presented to us earlier in this thread.
As far as I am aware, this is the first time that you have qualified this issue by using the word 'commonly'.
If you had done so before then that would have been helpful and accurate.
I'm pretty certain that it has been stated on this thread that people with historically defined ME do not recover, without qualifying the statement with the word 'commonly' or 'usually'.
And now we find out that, according to the Ramsay literature, some people with ME do recover... This is one example of how the facts seem to have been misrepresented.

You did suggest that I look at the historical literature, and this is what I have done, and in doing so, I discovered that it doesn't coincide with some of the information that some people have presented.
I will start reading the more up-to-date research soon, and it might be the case, that it all completely coincides with your info.

As for the assertion that it is always or can only be acute onset......
I dont believe that statement to be contradictory to the over all evidence (body of collective historical ME literature) which I understood the statement to be reflective of.

Thanks, I will look into this.

I am sorry Bob, I disagree strongly with this and for reasons already pointed out in my previous posts. When you take something out of context - be a paragraph to highlight a point, or *one* document- out of its known historical understanding, then it will, as here *appear to be making the case you suggest. Again I refer you to my post #90.

Well, I quoted three high profile papers of Ramsay's. And I've yet to see him say that fatigue is not the predominant feature of ME.
In terms of other research literature, it might be different, but Ramsay seems to be absolutely categorical about this.
Maybe the up-to-date research coincides with the information that you have presented.

Welcome to the world of medical science Bob, where outcomes are seldom 100%.

Its like the XMRV studies. Lombardi et al findings when first published cited 67% finding in its cohort. This was regarded as very significant and prompted further research and with it came the Alter Lo study. And this prompted further studies and so, in time, a body of literature builds to support general rules and propositions.

It is no different with enteroviruses and the vast body of literature on historic ME a lot of which was recorded in relation to over 64 epidemics. From it comes a general and strong body of evidence from which general rules are formed. There are always the odd exception, but they are not usually a focal point in medicine- the general rule is.

I accept that enteroviruses have been associated with ME, but what I'm questioning is the general idea that you can only have ME if you have an enteroviruses. I think that this is an important point to understand. I will keep reading.

I think people are doing their best Bob, within the limits of time and health.

I'm not ungrateful for people's time and effort.

But after being presented with such absolute 'facts' time and time again on this thread, it is a little bit surprising, to then find out that these 'facts' are not actually irrefutable facts, at least according to one of the highest profile authorities on ME.

If it turns out that the latest research completely contradicts Ramsay, then I will of course make it clear that none of the facts have been misrepresented, and I will apologise for suggesting that. But at the moment, I can only interpret and present what I have read so far.

I hope this makes sense and is not too repetitive. Its late here and I need to rest.

I will come back to reply to your other posts soon.

Yes, thanks, it makes sense. I'm going to have a break now as well. I'll return when i've done some more reading of the more up-to-date literature.

 

[insearchof]

Hi Bob

I have caught up now, and my statement was entirely correct, as outlined in my previous post. It is your statements that do not coincide with any of the Ramsay literature that I have read from 1986 or 1990.

I am sorry Bob, my comprehension of the article (1986) appears directly at odds with your own. Nothing more to say there.


Further, I note you say nothing about the historical context relating to the article which I point to at post #90 - that it fell within a confusing PVFS /ME mish mash period, which Ramsay subsequently acknowledged that his own errors there and emphasis - had contributed to and that this made things confusing. He went to great lengths subsequently to correct such.

Some of the facts have been misrepresented in this thread, at least as far as the facts relate to Ramsay, who is considered an authoritative source.

So far, I have seen one matter which was a matter of semantics, but was not a wild departure from the general body of literature and all the material I have read on the matter.

As for misrepresentations relating to Ramsay on this thread, what precisely are you referring to? Semantics? Small errors that were subsequently clarified? Facts that have been presented and supported here - that you simply do not view the same way? Is that a misrepresentation? If so, could it not be equally said that your views of the matter, and small errors, amounts to such to those of us that support the historical literature? I would not make such a statement or use the word especially in this thread, because I think the word ''misrepresented'' is too strong and suggests an intent to do so. Perhaps that was not your conscious intent and you used the word casually. All the same, I think it might be best for you to clarify this, as if left hanging, it might suggest to some passing by this thread, that some here are trying to rewrite history and that, I think - is rather troublesome.

If you could clarify this matter, I would very much appreciate it.

Must go. Will return to address your remaining posts later.

Thanks Bob.

 

[Bob]

Sorry Bob, I should have said that it is not possible to find enteroviral infections 100% of the time, for reasons already stated. Not that they are not always associated with ME, because the literature points to the fact that they are - especially the literature detailing over 64 epidemics which makes the case strongly. From that literature comes a general and strong body of evidence from which general rules are formed. There are always the odd exception, but they are not usually a focal point in medicine- the general rule is.

Today (with Chia's stomach biopsy test) we should theoretically be in a position to show enteroviral presence in an ME co hort without the difficulties of the past associated with serology and stool analysis. Of Chias patient base, I recall reading somewhere that he spoke of 80% of his patient base as enteroviral postive ME and the remainder have other viruses and causes which he refers to as he CFS patients.

You've edited your previous post, so i'll just respond to this point briefly.

Thank you insearchof... Your presentation of the information is far more nuanced in this quote than many of your previous statements... That is very helpful.

 

[Bob]

Hi Bob


I am sorry Bob, my comprehension of the article (1986) appears directly at odds with your own. Nothing more to say there.


Further, I note you say nothing about the historical context relating to the article which I point to at post #90 - that it fell within a confusing PVFS /ME mish mash period, which Ramsay subsequently acknowledged that his own errors there and emphasis - had contributed to and that this made things confusing. He went to great lengths subsequently to correct such.

Well, Ramsay repeats himself in 1990, in relation to fatigue and ME, and I think he died in 1990 didn't he? So he seems to be of the same opinion very late in his career.

But we can disagree about this, and let other people make up their own minds about this issue.

I do acknowledge what you said about the "confusing PVFS/ME mish mash period", but I am only dealing with papers by Ramsay right now...
I will acknowledge anything that contradicts Ramsay in my further investigations.
I am not biased in any way about this... I don't have any agenda here except to establish the facts, and I am just presenting the information exactly as I find it.

So far, I have seen one matter which was a matter of semantics, but was not a wild departure from the general body of literature and all the material I have read on the matter.

As for misrepresentations relating to Ramsay on this thread, what precisely are you referring to? Facts that have been presented and supported here - that you simply do not view the same way? Is that a misrepresentation? If so, could it not be equally said that your view of the matter amounts to such those who have read more widely? I would not make such a statement or use the word, because I think the word ''misrepresented'' is too strong and suggests an intent to do so. Perhaps that was not your conscious intent and you used the word casually. All the same, I think it might be best for you to clarify this, as if left hanging, it might suggest to some passing by this thread, that some here are trying to rewrite history and that, I think - is rather troublesome.

If you could clarify this matter, I would very much appreciate it.

Must go. Will return to address your remaining posts later.

Thanks Bob.

The issue that I have raised is that the facts have been presented in an absolute way, and they do not coincide with Ramsay's literature. If the facts do not coincide with the historical literature on such crucial points that I have highlighted, then I can't see that they can be presented with such absolute certainty. I would be surprised if the latest research contradicts Ramsay on so many crucial issues relating to the definition of ME. But I have acknowledged that I have further reading to do.

Like i said, if I find that the latest literature coincides with what has been presented in this thread, then I will be happy to confirm that.

I used the word 'misrepresented' carefully, not casually.
It does not imply that people are willfully or purposely attempting to distort the facts.
It only means that the information has not been 100% accurately presented, if the literature by Ramsay is accurate. Maybe I have been premature in saying this, but I have yet to see any evidence that I am wrong.

 

[Bob]

Ramsay 1986 definition of ME:

Muscle phenomena

[Fatiguability]: Muscle fatigability, whereby, even after a minor degree of physical effort, three, four or five days, or longer, elapse before full muscle power is restored and constitutes the sheet anchor of diagnosis. Without it I would be unwilling to diagnose a patient as suffering from ME, but it is most important to stress the fact that cases of ME or mild or even moderate severity may have normal muscle power in a remission. In such cases, tests for muscle power should be repeated after exercise.


Ramsay 1990 defintion of ME:

The cardinal features, in a patient who has previously been physically and mentally fit, with a good work record are:

1.Generalised or localised muscle fatigue after minimal exertion with prolonged recovery time.

 

[Bob]

Just to clarify, I would personally prefer to use the word 'exhaustion' rather than 'fatigue', or some other description of the illness. I am just presenting what the literature says, in order to establish the facts about historical definitions of ME.

I can't find a later definition of ME after Ramsay 1990, other than Nightingale.
Does anyone know if there are any?

 

[Bob]

Now onto the Nightingale Definition...

http://www.nightingale.ca/documents/Nightingale_ME_Definition_en.pdf

At the start, there seems to be a problem with the Nightingale definition, as far as I understand, that the definition is not published...
So should it be considered authoritative?

Byron Hyde definitely moves away from the using the term 'fatigue', which I think he doesn't even mention once in the Nightingale definition.
His statements coincide with what has been said on this thread about fatigue: "Fatigue was never a major diagnostic criterion of M.E."
I don't understand how that can be the case after the quotes that I provided from Ramsay's papers. I suppose that a diagnostic criteria is different to a description of the illness. Ramsay definitely talks about fatigue in both his 1986 and 1990 definitions (see my earlier post.)

Hyde seems to talk about 'loss of muscle function' instead of 'fatigue' or 'post exertional malaise':
"Testable Muscle Dysfunction: This feature may be due to vascular dysfunction or peripheral nervous or spinal dysfunction and includes both pain and rapid loss of strength of muscle function after moderate physical or mental activity."

Hyde does seem to think that ME patients can experience 'recovery', although it isn't clear to what extent:
"Extent of Injury:
Type 1: One side of the cortex is involved. Those patients labeled as 1A have the best chance of recovery."

Here is what Nightingale says about the cause of ME:
"Under epidemic and primary M.E. there is no consensus as to the viral or infectious cause. Much of this lack of consensus may be due in large part to separate acute onset from gradual onset patients in the M.E. and CFS groups of patients. Primary M.E. is always an acute onset illness. Doctors A. Gilliam, A. Melvin Ramsay and Elizabeth Dowsett (who assisted in much of his later work,) John Richardson of Newcastle-upon-Tyne, W.H. Lyle, Elizabeth Bell of Ruckhill Hospital James Mowbray of St Marys and Peter Behan all believed that the majority of primary M.E. patients fell ill following exposure to an enterovirus. (Poliovirus, ECHO, Coxsackie and the numbered viruses are the significant viruses in this group, but there are other enteroviruses that exist that have been discovered in the past few decades that do not appear in any textbook that I have perused.) I share this belief that enteroviruses are a major cause."
...
"Recent publications by Dr. J. R. Kerr have also identified the fact that enteroviruses are one of the most likely causes of M.E. If this belief is correct, many if not most of the M.E. illnesses could be vanquished by simply adding essential enteroviral genetic material from these enteroviruses to complement polio immunization."
Note that he does not say that enteroviruses are the cause of ME, but he says they are "a major cause".

And this is what he says about gradual/sudden onset:
"Under epidemic and primary M.E. there is no consensus as to the viral or infectious cause. Much of this lack of consensus may be due in large part to separate acute onset from gradual onset patients in the M.E. and CFS groups of patients. Primary M.E. is always an acute onset illness."
I'd like to see what evidence he bases his assertion on here.

Interestingly Hyde says this:
"Diffuse Brain Injury Observed on Brain SPECT: If the patients illness is not measurable using a dedicated brain SPECT scan such as a Picker 3000 or equivalent, then the patient does not have M.E."
So he asserts that all patients can be diagnosed using a SPECT scan.

 

[Bob]

There are still some discrepancies between what Byron Hyde says and some of the information that has been presented on this thread in relation to historic ME, although far less than with the Ramsay literature.

No discrepancy:
Hyde does not mention 'fatigue' and, as far as I can see, has replaced 'fatigue' and 'post exertional malaise' with 'loss of muscle function'.

A possible discrepancy:
Hyde does believe that 'recovery' is possible, but I'm not sure to what extent.

A sort of discrepancy with some of the posts:
Hyde does not say that all patients have an enterovirus infection, but says: "I share this belief that enteroviruses are a major cause."

Half a discrepancy:
Hyde does assert that "Primary ME" can only be sudden onset: "Primary M.E. is always an acute onset illness."
He also talks about a "Secondary ME", which he asserts is caused by toxic chemical injury, and so I suppose he believes (because he qualifies the above statement by saying "Primary ME") that this can be slow onset, although he doesn't state so explicitly in this paper. (I need to look for more info on what he refers to as "Secondary ME".)

No discrepancy:
Hyde asserts that ME can be diagnosed with 100% accuracy with a SPECT scan.


So, the info presented in this thread corresponds to Hyde's literature far more than to Ramsay's literature.
But some of Hyde's information is still more nuanced, than some of the info presented earlier in the thread.

Personally, I'm not sure what to make of Hyde's information yet... It's quite a departure from what I'm familiar with, so it will take me a while to understand it properly, and to look at the evidence that he bases his definition on.