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

[insearchof]

I agree!

The problem is also getting a treatment for whatever it is that we have (ME or no-ME).

I believe that if the "historical ME" patients stick with us (the CCC population), they will benefit from the research that is being done on us - something positive will come out... and for both groups.

Unfortunately, the research that comes from CCC does not relate to ME. The group caught under CCC is too varied. Even if they studied those that appeared closest to people with ME as defined by historic ME literature, there would always be a question as to how suitable, effective and or safe that research would be for ME patients.

The analogy you make is kind of like suggesting that ME patients should look at MS research, Cardiovascular research, Endocrine research and pick out the little bits that they think might have some general information there that they might like to consider, but which is not really usefull because it is not really specific to ME.

For example lesions found in MS are different to the Lesions found in ME. What is going on in the brain of MS patients appears to be something different to what is going on in ME patients.

 

[insearchof]

Hi Floydguy

I didn't mean there might not be many ME patients. I meant as a percentage of those diagnosed with CFS. I can't believe it's higher than 20-25%.

I think it's pointless to start with the average MD. The emphasis should be on the research end and who the research population is. Even though I probably don't have ME I feel I like the potential for breakthroughs are going to come from studying real ME patients as opposed to the ones researched by the CDC, Chalder, Wessley, etc.

For the life of me I can't figure out why anybody would want to have the CFS label slapped on them. I've been trying for several years now to get it removed!

I think the ME criteria outlined on this thread is probably better than CCC.

Focusing on and lobbying for ME research is definitely needed. However, researchers need to have some general understanding of what it is.

Further, physicans also need to understand - in order to diagnose and apply the findings of the research. They would also, presumably - be the ones who would provide the ME patient co horts for researchers.

I dont think the ME criteria is better than the CCC one - simply because one relates to ME and the other to CFS.

It is like comparing apples to oranges.

 

[fla]

This sounds like a very interesting thread but too long for some of us to read. When conclusions are reached if someone could summarize especially how to know if you have historical ME or something else. Also what treatment should be tried or avoided in either case.

 

[insearchof]

Hi Fla

I understand about long threads

There has been a suggestion that an area be created in the forum for general topics relating to historical ME.

If that takes place, maybe this thread and relevant parts of it can be divided up - for easy reference and reading purposes.

 

[Bob]

I dont think the ME criteria is better than the CCC one - simply because one relates to ME and the other to CFS.

It is like comparing apples to oranges.

I don't think that this is an accurate analogy, because of the overlap of the two. The CFS diagnostic criteria would probably include all ME patients. Well, that's unless doctors were to view 'ME' as an exclusion criteria for a 'CFS' diagnosis, which doesn't happen in reality. So, in the real world situation, Ramsay 'ME' is probably a subset of 'CFS', even if it's not supposed to be.

I think that there must be a lot of 'CFS' research material from the past 20 years that is relevant to 'ME'. Or at least research material that 'ME' researchers can build upon. The XMRV research is just one example that might be relevent to the historically defined 'ME'.

 

[Bob]

insearchof, one thing that i think you might be overlooking when you talk about the 'ME' research and history, is that no science is set in stone, and it might have been the case that if 'ME' research had been allowed to freely develop over the years, on a large scale, then the definitions might have evolved to include a wider spectrum of symptoms and patients. Or subsets of ME might have been created.

For example, we don't actually know if someone diagnosed in an outbreak area and who fits the historic 'ME' definitions, has a different disease to someone who has flu-like symptoms and became ill sporadically with a slow onset illness, whose main symptom is fatigue or pain.

We don't know because we don't know the cause of either sets of symptoms, and maybe not enough research has been carried out on both sets of patients to compare the physiological similarities, if there are any.

 

[Tulip]

It is my belief from nearly 20yrs of observing, that a number of people diagnosed with CFS, actually have Fibromyalgia instead. The pain, fatigue, brain fog, sometimes sore glands, ibs and sometimes food intolerances. FM fits into the CCC criteria as well and all other CFS diagnostic criterias, but not the M.E. one.

 

[insearchof]

Hi Bob

I don't think that this is an accurate analogy, because of the overlap of the two. The CFS diagnostic criteria would probably include all ME patients. Well, that's unless doctors were to view 'ME' as an exclusion criteria for a 'CFS' diagnosis, which doesn't happen in reality. So, in the real world situation, Ramsay 'ME' is probably a subset of 'CFS', even if it's not supposed to be

There might be an overlap in relation to one or two symptoms -but they are in all other respects drafted from different supporting med lit sources and for two different illness groups.

The CFS diagnostic criteria is very different from the historic ME literary one. That is not to say that CFS as defined, will not presently catch ME patients. It can and does, but that is primarily due to a physicans lack of knowledge and understanding on what historical ME is.

ME is an exclusion to a diagnosis for CFS. Sadly though, you are correct - it seldom happens for the reason previously arrticulated.

In the real world, ME patients have been mis diagnosed. The term sub set used in association with CFS -should not be used to historic ME, as it cannot be supported on the scientific literature and only serves to obscure the distinctions, that this thread is trying to make.

The real world, is also one that both ME and CFS communities are tyring to change - because it is clearly factually and scientifically flawed.

 

[insearchof]

Hi Bob

insearchof, one thing that i think you might be overlooking when you talk about the 'ME' research and history, is that no science is set in stone, and it might have been the case that if 'ME' research had been allowed to freely develop over the years, on a large scale, then the definitions might have evolved to include a wider spectrum of symptoms and patients. Or subsets of ME might have been created

I understand that science, like most other things in life - evolve.

Medicine, as I understand it with the aid of research, generally hones in on understanding the operation of aspects of a disease and how it applies to its defined class. I dont really know of too many branches in which research has expanded the class of patients to whom the set and distinctive symptom list applies.

For example, we don't actually know if someone diagnosed in an outbreak area and who fits the historic 'ME' definitions, has a different disease to someone who has flu-like symptoms and became ill sporadically with a slow onset illness, whose main symptom is fatigue or pain. We don't know because we don't know the cause of either sets of symptoms, and maybe not enough research has been carried out on both sets of patients to compare the physiological similarities, if there are any

According to historic ME literature, one of the key diagnostic criteria of ME is accute or sudden onset. The example you cite is a difficult one.

In your example you cite an identifiable accute onset event (flu like illness) which has been recognised in the historic ME literature.

You then state that there is a slow manifestation of symptoms. What does that mean though? Does it mean that the patient has recognised symptoms found in ME literature but did not have as many as some of the more severely affected ME patients? If so, that does not exclude the patient from a diagnosis if the patient meets the criteria in all other respects.

Yet if that patients main symptoms are pain and fatigue, without the symptoms necessary to assign an ME diagnosis - then yes that individual is unlikely to have ME.

In which case we can clearly say that whilst their cause of their illness may not be known - the cause of illness in ME, as outlined in historical ME literature is known. The cause of primary ME is generally regarded as enteroviral infection.

 

[Bob]

Thanks insearchof, for taking the time to respond to the points that I raised... It's much appreciated.

In which case we can clearly say that whilst their cause of their illness may not be known - the cause of illness in ME, as outlined in historical ME literature is known. The cause of primary ME is generally regarded as enteroviral infection.

OK, I didn't know that this was quite so clear-cut. I thought that the cause attributed by the historical definitions of ME had been opened up over the years, beyond just being due to an enterovirus, and that other possibilities of causation had been considered. I've still got a lot more to learn! And I'm working on it. Slowly.

 

[Bob]

Thanks rlc, for another interesting and helpful (and long) post, which i've finally managed to read.
There's just a few points that I'd like to highlight, and respond to...

This is a major difference between the Nightingale and CCC definitions. Dr Hydes definition explains how to 100% accurately diagnose ME whereas the CCC leaves it as a guess!

That's interesting food for thought!

The CCC also doesnt actually say you have to have PEM, it sayss this
There is an inappropriate loss of physical and mental stamina, rapid muscular and cognitive fatigability, post exertional malaise and/or fatigue and/or pain and a tendency for other associated symptoms within the patient's cluster of symptoms to worsen. There is a pathologically slow recovery period. usually 24 hours or longer.

I'm not sure if I totally agree with you here. If the term Post-Exertional-Malaise was replaced with Post-Exertional-Relapse, then it would demonstrate how ME/CFS, as I know it, has a unique type of reaction to exertion. The last sentence in the above quote demonstrates this uniqueness of ME/CFS, as I recognise it personally, which is "a pathologically slow recovery period. usually 24 hours or longer." I don't know if you'd agree with this at all? Unfortunately doctors can't distinguish between different types of fatigue, as the patients can, even if the doctors are instructed to, so I acknowledge that describing the nature of PEM or PER in diagnostic criteria might not be helpful to distinguish ME patients.

So to sum it all up the Nightingale definition which is written by Dr Hyde who has worked exclusively with ME patients for a quarter of a century, in Canada and all over the world, who has read all the published and literature pre 1988, and has personally gone and examined patients from all but one of over sixty of the known ME epidemics.

That's very interesting... I didn't know that Hyde has visited patients in every single outbreak area (except one), and I didn't know that there had been over sixty areas. It interesting that he must witness exactly the same set of symptoms in patients in each outbreak area, for him to stand by the definitions of 'ME' so staunchly..

Thanks very much for all of this information.

 

[insearchof]

OK, I didn't know that this was quite so clear-cut. I thought that the cause attributed by the historical definitions of ME had been opened up over the years, beyond just being due to an enterovirus, and that other possibilities of causation had been considered. I've still got a lot more to learn! And I'm working on it. Slowly

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.

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

 

[insearchof]

This is a very interesting thread and I have learned a lot. However, I don't feel comfortable participating in it anymore and telling why would cause a lot of problems on this post. So, I prefer to withdraw myself from this discussion at this point.

Hi Boule de feu

Bob has withdrawn his questions and given what you have written, I have elected not to respond.

I hope this remdies any discomfort you might have otherwise been feeling and that you will re join the dicussion. If not, that's ok - maybe you can jump in at a later date?.

 

[Boule de feu]

Hi Boule de feu

Bob has withdrawn his questions and given what you have written, I have elected not to respond.

I hope this remdies any discomfort you might have otherwise been feeling and that you will re join the dicussion. If not, that's ok - maybe you can jump in at a later date?.

To the contrary, I would love to hear what you have to say. I'm glad that Bob did ask this question. I am very curious to find out how it works to get a diagnosis of "historical ME". I think it would be helpful to others like me. I know it would lead me in the right direction. I could ask the right questions to figure out what my diagnosis is. And if I am lucky, I could find out what it is that I am suffering from.

 

[insearchof]

To the contrary, I would love to hear what you have to say. I'm glad that Bob did ask this question. I am very curious to find out how it works to get a diagnosis of "historical ME". I think it would be helpful to others like me. I know it would lead me in the right direction. I could ask the right questions to figure out what my diagnosis is. And if I am lucky, I could find out what it is that I am suffering from.

Hi Boule de feu

I am a little bit confused Boule de feu.

I see that your post (which was #196) which quoted Bobs questions to me (which he deleted/withdrew after your quote -at what was #195) - you have now deleted.

Prior to deleting your post where you quoted Bobs questions to me - you stated that you were uncomfortable with continuing on this thread because you felt that what you knew would cause problems on that post ( I took to meaning Bobs questions and my replies).

However now you say that on the contrary, you are glad Bob asked and would like to hear my reply. Hence my confusion.

In any event - Bob asked how long I had been ill, in order to know so much about historical ME.

He said that if I did not feel comfortable about answering that question or about my health that I should not do so.


So all I will say to you is this.

I dont see how the duration of my illness has any relevance to the degree of my knowledge or understanding on the subject matter of historic ME.

Also, I dont see how an answer to that question will assist you or anyone else in knowing the right questions to ask, or finding out how it works to get a diagnosis of ME as outlined in the Nightingale document.

It really isnt relevant to the questions you are now asking.

However, with regard to the questions you now ask, I am sorry Boule de feu, but I will not discuss my personal medical history or personal details on a public online forum - if that is what you were wanting me to disclose. I have a note to this effect on my visitors page which has been there for some time now. It is not something I am comfortable with at all - either on or off line for that matter.

The simple answer to your question however, given you live in the same city as Dr Hyde - Ottawa Canada, is to consult him. Alternatively, if you cannot afford to do so, ask him for a referral to someone who can. In the early days of the Nightingale Foundation, I believe he had other knowledgeable doctors working with him in this area and conducting research. Maybe he could refer you to one of them. You of all people are very fortunate to reside in his home city and it should therefore be easier for you, than most others, I would have thought.

Alternatively, there is a post somewhere in the forum made by RLC - which might be useful to assist you and others on answering your questions. I will see if I can find it - if you or anyone else is interested. If you are still interested, let me know.

 

[Boule de feu]

Hi Boule de feu

I am a little bit confused Boule de feu.

I see that your post (which was #196) which quoted Bobs questions to me (which he deleted/withdrew after your quote -at what was #195) - you have now deleted.

Prior to deleting your post where you quoted Bobs questions to me - you stated that you were uncomfortable with continuing on this thread because you felt that what you knew would cause problems on that post ( I took to meaning Bobs questions and my replies).

However now you say that on the contrary, you are glad Bob asked and would like to hear my reply. Hence my confusion.

In any event - Bob asked how long I had been ill, in order to know so much about historical ME.

He said that if I did not feel comfortable about answering that question or about my health that I should not do so.


So all I will say to you is this.

I dont see how the duration of my illness has any relevance to the degree of my knowledge or understanding on the subject matter of historic ME.

Also, I dont see how an answer to that question will assist you or anyone else in knowing the right questions to ask, or finding out how it works to get a diagnosis of ME as outlined in the Nightingale document.

It really isnt relevant to the questions you are now asking.

However, with regard to the questions you now ask, I am sorry Boule de feu, but I will not discuss my personal medical history or personal details on a public online forum - if that is what you were wanting me to disclose. I have a note to this effect on my visitors page which has been there for some time now. It is not something I am comfortable with at all - either on or off line for that matter.

The simple answer to your question however, given you live in the same city as Dr Hyde - Ottawa Canada, is to consult him. Alternatively, if you cannot afford to do so, ask him for a referral to someone who can. In the early days of the Nightingale Foundation, I believe he had other knowledgeable doctors working with him in this area and conducting research. Maybe he could refer you to one of them. You of all people are very fortunate to reside in his home city and it should therefore be easier for you, than most others, I would have thought.

Alternatively, there is a post somewhere in the forum made by RLC - which might be useful to assist you and others on answering your questions. I will see if I can find it - if you or anyone else is interested. If you are still interested, let me know.

Thank you for your answer.
I will leave it at that.

 

[Bob]

Just for clarity, the personal question that I asked, and then deleted, was purely out of personal interest, and it was not meant to be used to shape the discussion in any way, not to judge any answers, nor intended to lead onto further discussions. It was an isolated question that I just asked out of curiosity. I hope I haven't embarrassed anyone.

 

[Bob]

I'd just like to say that I really appreciate the huge effort that so many people have put into this thread to share their knowledge.
I've learned a lot from it personally, and have found all points of view interesting and helpful.
I now need to print out some more of the historic 'ME' literature and definitions, to read more about the subject.

insearchof, thanks for your recent long post #195... I think i'll print it out and read it later this evening.

 

[insearchof]

Just for clarity, the personal question that I asked, and then deleted, was purely out of personal interest, and it was not meant to be used to shape the discussion in any way, not to judge any answers, nor intended to lead onto further discussions. It was an isolated question that I just asked out of curiosity. I hope I haven't embarrassed anyone.

Hi Bob,

No I am fine. Curiosity is healthy.

 

[sandgroper]

Last year I was fortunate enough to meet Dr Hyde in a small group setting. My story is not typical ME as far as I can tell, unless I take a second infectious incident as being the one that triggered the illness. WHen I tell my story I usually use an earlier incident which involved primarily a bacterial infection. Certainly after a brief discussion and look at some results Dr Hyde said I had obvious central nervous system dysfunction. I also have the body type he often finds and I have since been dx with EDS. What is not clear to me is whether I am an atypical ME type and if this is related to the EDS. He mentions them specifically in his definition but it is not clear to me whether he is saying that this type is different from the epidemic type. Hope that makes sense.
Sandgroper