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

Discussion in 'Action Alerts and Advocacy' started by Tulip, Apr 9, 2011.

  1. insearchof

    insearchof Senior Member

    Hi Cort

    If your suggesting that ME and PVFS, needs to be weeded out of CFS discussions and literature, I absolutely agree. But this needs to be tackled, in particular, by those in the CFS advocacy community. Will it take place there ''eventually''? Most likely, because it is taking place in other quarters and has been for a while now.

    You see, the CDC recognise the distinctions or at least that ME and CFS are not the same and state so on their web site.

    You have the CCC that makes no reference to ME as we know it from the historic literature possibly because they were attempting to summarise the findingd of CFS research ( for the purposes of assisting in clinical diagnoses) and were, in so doing - probably also acknowledging the existing distinction.

    You have the Nightingale Institute of Canada, you have doctors like Dr Miraz, Dr Hyde, Dr Dowsett, Professor Hooper and you have groups like HFME and ME advocates raising awareness on the matter.

    I can understand why you would think this discussion might get in the way of advocacy though.

    Whilst I agree with you, that CFS has had what you refer to as ''piddly'' funding over 25 years - this fact - has had an adverse effect on ME as well, with it receiving no funding at all.

    Cort, there is genuinely a lot of fascinating reading to be found in the historic ME literature as well as in earlier discussions in this thread, including the point on prognosis and recovery in ME. See here and

    The papers findings are not that fascinating in the context of the general body of historic ME literature.

    In terms of a comparative analysis between Dr Bells studies or other CFS studies to ME, there might be (as with many illnesses) points of similarity between a certain subset of patients with CFS with ME. However, it is important to note that similarity does not mean - the same as.

    As has been acknowledged in many shapes and forms both on this thread and elsewhere, ME and CFS are two seperate and distinct medical entities.

    Having said that, the subset in CFS that is similar to ME, could in point of fact contain ME patients as defined by the historical medical literature - who have been misdiagnosed with CFS.

    However, unless and until - the CFS community up holds the distinctions between the illnesses of the ilk we are discussing and acknowledging on this thread- they are unlikely to ever find out if that is indeed the case.

    It is important I think - both for that possible misdiagnosd subset of CFS who might have ME and for clarity of research generally, that this be done don't you think?
  2. taniaaust1

    taniaaust1 Senior Member

    Sth Australia
    Im one who says I had slow onset but in reality I dont know as I dont really know when it started.

    I had two incidences in my childhood where after excertion.. my leg muscles like went into pain and "ran out of energy" and I couldnt walk no more. (Once was while out shopping with my grandmother and the other time on a school hike.. I was a very fit and active child but on this day.. I suddenly found I couldnt walk any more, none of the other children have issues).
    I forgot about that thou and only just recently a couple of relatives reminded me of one of those incidences 25 years after the incidents. (I now do have vague memory of school hike incident, they told me about the other incident which had happened a few years before). The only other time I had issues during childhood was when I got mono as a teen and spent 10 weeks bedridden and extremely ill with it before I recovered. Something which I see as a bit abnormal is I NEVER caught a cold I can remember during childhood so never sick off school except for the mono (interesting many with CFS/ME dont seem to catch colds).

    As far as ME/CFS or whatever I have goes (11 years after the mono). I did just suddenly get very sick... well one day and sick the next (early flare trigger was run down immune system.. exams..lack of sleep, super busy. high stress periods). The thing is I was better a week later... Id got a "virus" of some kind. A month or two later it happened again.. same viral symptoms and spent another week in bed.. a month or two later.. same again. These incidents got closer and closer together...till I knew i couldnt be catching a virus all the time. After 9 mths of "mystery virus" on and off I did realise I had CFS... a short time later I was bedridden completely for 9mths (that crash took many many years to recover from.. doctors told me I'd recover in 2-3 years, I think they thought I had Post Viral Syndrome.. but it took me many more years then that till I went into my one and only remission Ive had). I was tested for a lot of different viruses.. everything negative there but my first 9mths of symptoms fit a reactiving virus

    So was I slow onset or fast. Was it CFS/ME the very first time I got hit with viral "flu like" symptoms which did put me in bed for a week? Well one day and sick the next...but I felt well a week after and was for a month or so before it hit again (same triggering thing) does that count? as the start? or do I say I got the CFS/ME once it had set permanently in.. with no well days.

    I like many are confused as many others on what onset we have.. but I did go from a healthy well person into someone who was sick in bed the next day with up glands, high fever, muscle aches (I looked like a bull frog as I all puffed up under eyes too) but being on and off illness at first.. can one say that was sudden onset?. (Symptom intensitiy wasnt slow.. something different about my case to what I read about ME was my fevers were very high ... (i also got super high fevers causing unconsciousness when I had mono as teen so maybe Im just more prone to very high fevers when sick).

    Maybe Im actually a post viral syndrome case??? Thou Ive once read that that only lasts 2-3 years. I first got CFS/ME 14 years ago (with a 2-3 year remission after the first 5 years). I guess I should read up more on post viral syndrome and see if I seem to fit that defination or not.

    Does anyone know the offical post viral fatigue definition?
  3. insearchof

    insearchof Senior Member

    Hi Tania

    This struck me as reminiscent of mild accounts of polio in children I have read about:

    Do you know how old you were and whether this incident coincided with any of the following:

    *oral polio vaccine or booster?
    *were you around anyone else - friend, relative, school chum - who succumbed to polio?

    Richard Bruno (Director of Post Polio Institute) talks about mild cases like these too (if my memory serves me) and how years later you can come down with Post Polio Syndrome
    which he has written about being similar to CFS.

    The acute -v- sudden onset thing can be tricky to work out - as stated. Good investigative physicians like Hyde and Chia can sort through it though. Having said that, this sound like an acute onset of something:

    Enteroviral triggering illnesses are usually of a short duration - 3-7 days on average.

    I have also read (again I think in Bruno's work) that some patients who came down with one type of polio enterovirus, also later came down with another enteroviral infection.

    So it would seem that some people are not only susceptible to enteroviruses, but some are also susceptible to being reinfected by other strains as well.

    Even if you did not have a polio event in childhood, it does makes me wonder if you had an enteroviral infection back then anyhow. Some of, what are referred to today as non polio enteroviruses, can also cause leg weakness/paralysis. If so, did that set up your immune system for mono and did you get a subsequent enteroviral infection, that triggered your current illness?

    Would be interesting to know.

    In terms of PVFS - that area is a mess. Ramsay's literature is probably the best source - but the accessible information (online) only has little bits and pieces in it that you need to pull together. I might do that and post it, because I did say to Bob, that I would revisit some of the Ramsay ref he posted.

    If you are interested in the subject though, you might want to see if you can get a copy of Ramsay's book: ME and Post Viral Fatigue States: The Saga of the Royal Free Disease (1988). I have not read that book, but I imagine it would be very useful.
  4. insearchof

    insearchof Senior Member

    XMRV and ME

    Hi rlc and everyone else participating in this thread.

    I wanted to post a follow up on your comments rlc, with regard to XMRV and ME.

    As I have always been careful to look at what research definitions have been applied, I came to the same conclusion that you did - that XMRV is associated with a CFS co hort (CCC and Fukuda) and not ME.

    I think it is very important that this be noted, for no other reason than what we have been discussing through out this thread - the importance of making the distinction between ME and CFS and the need to maintain it and preserve what is known and understood regarding historical ME.

    I agree, that the case for causation in ME - is and has historically been associated with enteroviral infection.

    All the same, I am very interested in and am keenly following the science in relation to XMRV and CFS.

    My own personal view on XMRV is :

    *That Alter Lo teams work vindicates the findings of Lombardi et al
    *A true replication study of Lombardi et al remains outstanding
    *A number of explanations raised for lombardi et als findings (by negative studies) have not been successful in their assertions (Bob did a great summary on this on another thread recently post 223
    *That a number of other positive studies are yet to be published together with other material in support of Lombardi work
    *There is evidence of sequence variation in XMRV (expected to be found in viruses ) which WPI are trying to have published and accepted in GenBank
    There is evidence of DNA integration of XMRV in prostate cancer cells

    Further, it is not the first time that a retroviral association has been mentioned in regard to CFS which began back in 1986 and were aborted because of a lack of funding.

    Clearly symptom onset is a key differential between detecting an enteroviral infection and an XMRV infection as the studies you quote show.

    However, I speculate as to whether an asymptomatic XMRV infected person, may be made more susceptible to enteroviral infection because of the activation and presence of a retrovirus?

    Could this explain why only 5% of persons in the historic ME literature usually went down under an enteroviral infection that 95% of the remaining population did not succumb to? Could it be another immune assault (along with others that have been identified) that makes a person more susceptible to enteroviral ME? Is it possible that an ME patient had a pre existing retroviral infection that had a negative synergistic relationship with enteroviruses?

    Of course both retroviruses and enteroviruses are RNA viruses. Could it be that one (ie retrovirus) makes the other (enteroviruses) more potent than might otherwise be the case (ie 95% of the population dont get ill from enteroviral infections)?

    Believe it or not, it appears that retroviruses have been speculated to play a role in ME and were written about in relation to ME, as early as 1959.

    Apparently, in 1959 Dr Bjorn Sigudsson from the Institute for Experimental Pathology in Iceland wrote on Icelandic Disease (ME outbreak in 1950s) conceiving the idea that more than one viral infection might have been involved. In particular, he referred to the visna retrovirus found in sheep. This was thought to be the same as the retrovirus found by Dr Michael Holmes in 1986 in a CFS cohort. Dr Sigudsson stated that this retrovirus could take a long time to do its damage. On his deathbed he dictated his ideas on the association of this virus with the effects of Multiple Sclerosis. Further, Hyde in The Clinical and Scientific Basis of ME and CFS, (1992) in commenting on the uniqueness of the 1934 County General Hospital LA ME epidemic and Gilliams notes on it, also speculated as to whether a retrovirus may have been involved. Admittedly, that was in 1992 at the time of the Defraitis reterovirus discovery, which might explain Hyde's speculation there. However, I find the possibility kind of curious in light of this thread here: that might explain an retroviral connection with that ME outbreak back in 1934.

    So at this stage, I maintain a health curiosity and remain open to the possibility of both XMRV and its possible association in ME (although not presently shown) and am following the science in this area with interest.

    If XMRV pans out, I would like the WPI to study a pure ME cohort, possibly selected by Hyde, with enteroviral work ups by Chia :D
  5. Bob


    England (south coast)
    Hi tania,

    The way you have described becoming ill sounds like a possible pattern of acute onset ME to me...
    I've been reading some of the literature about the pattern of the illness, and they describe how some people get ill in the same way as you describe...

    I'm not referring to the leg paralysis when you were a child, as I haven't seen that sort of event described anywhere yet... But what insearchof says about it is very interesting... But I'm referring to your description of periods of flu-like illness.

    Here's some quotes that describe your experience exactly...

    Hummingbird website:
    " some cases, acute onset M.E. is preceded by a series of unrelated minor infectious episodes (in a previously well patient) which may be misinterpreted as being a gradual onset of the M.E."

    John Chia:
    "Many of them had frequent respiratory infection in the previous year ... ... before developing more fatigue.
    The case I presented at the symposium illustrated this principle. The patient developed a respiratory infection in November but did not have abdominal pain and onset of fatigue until May of the next year."
    "Furthermore, a number of patients would tell me the CFS started in March or April but could not even remember that they had recurrent bronchitis in the previous October through December."

    See longer quotes from them in my earlier post:
  6. Bob


    England (south coast)
    Fascinating... Thanks so much for that, insearchof.
  7. taniaaust1

    taniaaust1 Senior Member

    Sth Australia
    Interestingly ISO I took that article in a very different way to what you did.

    Thou he called it IVN along with calling it ME, he did say it wasnt like IVN due to their being many more symptoms... so I myself didnt precieve him as calling what would be classical kind of IVN, ME, as he was saying it was something a bit different.

    He makes it clear again here that IVN was just the term he'd called the epidemic he was studying by his quote "what I was calling" .. he didnt say it was IVN but just that he was calling it that. (I assume as at the time he didnt know what else to call the epidemic). So I didnt take him as calling what really was IVN ME (but just the thing he'd named that), so there is probably not much point in researching IVN to see if is like ME as it probably isnt going to be as what he was studying was different and not IVN. (thou Im now a bit curious myself about what this IVN is and IF it does appear in epidemics).

    Ive been trying to research epidemic neuromyasthenia (ENM) which was ME before the term ME happened (I was reading about the history of the name only yesterday and who made the name up but now cant remember where i saw it.. in 1950s both ENM and ME was being used for ME.

    The epidemic which he mentions (1949-1951 it was), happened about 30mins from where I live, (more accurately I think that was the Goolwa one rather then Adelaide to be more specific unless there was two near, a few years apart). The full study isnt online (can be ordered thou if you pay for it I think). but anyway here is an extract to it and those who support ME do recognise this in history as an ME outbreak .. and it does have vascular features..

    Clinical Description of a disease resembling poliomyelitis seen in Adelaide", (Pellew RAA) 1949-1951, Med J Australia, 1, 944
    Epidemic Neuromyasthenia (ENM)
    "Further investigations on a disease resembling poliomyelitis in Australia" (1955), Adelaide, Pellew RAA, Miles JAR, Med J Aust. Epidemics.htm

    "ME Research UK has funded research which has revealed abnormalities in the function of blood vessels and blood cells. Abnormalities of blood vessels have been described in these epidemics of ME/NM. Infectious material was transferred from patients to monkeys during an epidemic in Adelaide, Australia in 19491950. The monkeys became ill and post-mortem examinations were carried out a month later. The only abnormalities discovered by Pellew and Miles (1955) were minute red spots along the course of the sciatic nerves. Under the microscope the red spots contained localised collections of inflammatory cells, which had also infiltrated the area where the nerve roots come out of the spinal cord. The red colour of the spots was due to leakage of red blood cells. ME/NM is very rarely fatal so that a post-mortem study showing similar haemorrhages in humans is unique. However, during the North of England epidemic in 1955 Andrew Wallis described the findings in a patient in her fifties"

    and also in another outbreak which is recognised as an ME one "Vasculitis involving the skin was recorded during outbreaks in Cumberland, Durham and North West London in 1955. A maculopapular rash may appear during the return of features of the initial illness such as flu-like symptoms and enlargement of lymph glands and liver. This skin overlying areas of localised muscle weakness may be affected at the time of these attacks.

    So I think we can say that symptom of vascular issue is in ME (if not it means we have to discount history studies which are and were classified as ME and start calling them post viral syndrome or something).

    Now one has to ask oneself what did he see as the symptom of painful veins.. a clue to that comes with
    So maybe pain in legs which he thinks is coming from inflammed deep veins? Who knows but if one is interputing it like this.. it still sounds like common ME symptom most of us have and not something sounding unusual after all..

    Those severely sick (Im talking about bedbound patients) and I think we can agree that there are some very ill ME patients as some do die.. light coma states arent uncommon. So thou I havent found reference to it in the historical texts Ive read so far (im no expert on historical ME texts), Im sure this state of exhaustion so bad there is a heavy extreme sleep or like a light coma like state going on at times is a ME symptom.

    I know myself when I was in that state of light coma, I wouldnt have noticed bruising had I had it in the (**oh word loss opposite to chronic**) stage of my illness. I do know that Ive had bruising at times (not commonly thou) with the illness I had and dont know how I got a bruise.. shrugs maybe I did knock myself but didnt know?. (I also had the blood vessels in one of my eyes burst.. I dont know if that was related to my illness or not). According to those historical ME outbreaks with the vascular issues.. little haemorrhages would expect that there may be bruising at times with a symptom like that.
    I do think that with ME having so many different symptoms that it may be hard to find every one in the historical texts and all the experts often focus on different aspects (just like our experts nowdays tend to do). Everyone has written about it from their perspective rather then a consensus point. I personally think we can possibly get a even better view on it by studing various cases of it, throu all different ones who studied the outbreaks of it.

    I dont completely disagree with him as it is "generally" recognised by many that ME is nowdays commonly known as a subgroup of CFS and that ME is often called CFS. (yeah I do know it is incorrect but its just how things currently at this point of time.. with like CDC not "fully" recognising ME and going as far as putting up ME definitions etc. It isnt completely incorrect to say that ME is a subgroup of CFS till those like the CDC go and make things clearer. One can say the CDC recognises ME like you said.. but on the other hand it also kind of dont at the same time (if it did, it wouldnt do as it does and try to hide ME).

    I too will sometimes say CFS when refering to ME.. I think a lot of us do even those who know the that they can be very different things. I think most will recognise CFS epidemics as being probably ME.

    One needs to take that article as a whole and not be dicepting (sorry.. my ability to spell has left me right now and i cant figure it out) it. If taken as a whole, he clarifies what he means and one has to read article with that whole in mind. When he refers to IVN.. its his version of it.. an illness he just called it as he didnt know what the illness was at the time.. it isnt IVN.

    Keep in mind that he's viewing ME as a subgroup of CFS (that's my interputation), then it makes sense.

    I disagree, its how it was interputed, picking it to pieces and not seeing as a whole.

    I can thou see how some would be confused...

    We'll agree to disagree on the article :) . (I hope my post makes sense, Ive had a hard time doing reply). Thanks for the comments (I havent taken offense at anything just in case you wondered, just thought I should add that as sometimes Im interputed wrongly)

    For anyone wondering.. discussion is over what has come to be known as 1970s ME outbreak being discussed by a ME specialist who investigated it back then but then did the article on what he'd found in more recent times (hence why term CFS shows up at times in the article which is confusing some)
  8. Bob


    England (south coast)
    I realised that I hadn't explained why I had posted some of the info that I posted earlier/last night, so I've just added some introductory text to some of it.
  9. Bob


    England (south coast)
    In case it helps anyone... This is how to paste a link to a specific post...

    At the top right hand corner of each post is the post number - it's #369 for this post.
    If you click on that number, then it will direct your browser specifically to that post.
    You can then copy the internet address, from where your browser shows you which webpage you are in, and you can use that as a link to a specific post.

    Or, you can just right click on the post number (top right of the post = #369 for this post), and then click on 'copy shortcut', 'copy link location' or 'copy link address' and then 'paste' the link into a post.

    For example, this is the link directly to this specific post:

    Notice that towards the end of the url, it says 'post', which indicates that it is a link for a post - It then quotes a unique forum post number, which is '179191' in this case, but this number is not the same as the post number on the thread.

    Hope that helps. :confused:
  10. taniaaust1

    taniaaust1 Senior Member

    Sth Australia
    ah thanks.. Ive been told that before but kept on forgetting.
  11. Bob


    England (south coast)
    Well, it wouldn't be difficult to start a wiki page, and post the titles of, and links to, papers and literature.
    Two list could be made - one in order of the date of publication, and another under a list of names of authors.
    And I suppose a third list could be made that links each paper to a specific outbreak.

    It wouldn't be difficult to do, and I wouldn't mind collating and presenting the information.
    I could devote a bit of time to it, but not loads of time.

    Would anyone else be interested in helping to gather the links, and guiding me on how to collate the info?
    I couldn't do it all myself because I'm finding it hard to find the information. Lots of the Hummingbird links are broken.
  12. Bob


    England (south coast)
    Hi rlc,

    Thanks for your post...

    I think that there is a flaw in this argument... It could be possible that the underlying cause of ME is a dormant retrovirus (i.e. an MLV-related virus) but that the disease process needs to be triggered by an infection of some other pathogen, such as an enterovirus. It is said that viruses can interact with each other, changing the way that they act on the immune system.

    That's very interesting...
    So in the past, monkeys have been infected with ME by exposing them to the tissue or blood of ME patients...
    And after examining these monkeys, after death, they have shown disease in the tissues of the monkeys.

    I think this could tell us quite a lot, if futher up-to-date research was carried out on monkeys infected with ME tissue.

    And it would be interesting to compare them with monkeys infected with XMRV in comparison studies.

    (Although, as a personal note, I'd just like to mention that I totally disagree with most, or all, animal experimentation, particularly in monkeys. I find it deeply distressing, and I believe that it is unnecessary most of the time.)

    You say that no disease was apparent in the monkeys recently infected with XMRV, but that's not what I remember reading. I'm pretty sure that I read that the monkeys had displayed signs of illness before death. But I didn't read about the nature of the post mortem investigations.

    I think we would have to study the literature closely, before we can draw any conclusions from a comparison of the post mortem investigations in the two different experiments...
    For example there maybe differences in how long the monkeys were infected for, before they were killed...
    And the XMRV study may not have been looking for the same sort of damage...
    They might just have been looking for the XMRV in the tissue, and not what damage it caused.
    (I haven't looked at the details of post mortem investigations of the XMRV-infected monkey studies.)

    There would need to be proper comparable studies before we could draw any conclusions.

    I disagree with a lot of what you have said here.

    I think that the WPI has studied some patients from outbreak areas because they have researched ME patients from well known ME doctors in the USA.

    Although it is correct that the WPI do not use historic 'ME' diagnostic criteria, they are aware of the differences in patients exhibiting neurological and immunological symptoms, to patients who only have fatigue without the other symptoms.

    So, assuming that the CCC and CDC criteria do not filter out ME patients (which I do believe), then the WPI have their own way of selecting a subgroup of patients with neurological disorders.
    So to say that the WPI only uses the CCC or CDC criteria is not strictly correct, as they do further selecting.
    Whether they actually select ME patients is up for debate, but in my opinion, they probably do, based on the symptoms of the patients that they select.

    When you say that XMRV is just a retrovirus, and is easy to detect, I couldn't disagree more...
    XMRV was only detected for the first time in 2006 (in prostate cancer patients.)
    Very little is known about the virus, with most scientists only just beginning to agree that it is indeed a human virus.
    The CDC are unable to detect XMRV in the blood of any XMRV-positive prostate cancer patients, even though they agree that some of the patients are indeed infected.
    So XMRV appears to be extremely difficult to detect, and established methodologies appear to be unable to detect it, as all of the zero/zero studies might indicate.

    I'm enthusiastic but open-minded about the XMRV research, and I would be equally interested in seeing enterovirus research given the same prominence.
  13. insearchof

    insearchof Senior Member

    Hi Tania

    I went back and reconsidered the article, but I have to say at the outset, that I still found his use of terminology confusing and not very helpful to me personally. But that might just be me.

    I personally believe he was saying IVN was the same as ME (which is why I was troubled and made my initial post) because he makes the following remarks.

    He clearly distinguishes INV from EP but not ME, on the basis of IVN having many more symptoms than EP but not ME.

    In the next sentence then goes on to state that it is indeed similar to ME but notes that few vascular features are mentioned in ME

    So at this point he is saying it is similar to ME but not the same because of the fact that very few vascular features were mentioned in the ME literature . I agree with him here.

    He then goes on and states that what he calls IVN, is a ''variant of the Chronic Fatigue Syndrome'' that he specifically states was called ME before 1988

    So he clearly states here that what he terms IVN is the same as ME, albeit a variant of it.

    He then goes on to discuss the Pellew and Miles study of an ME epidemic in Adelaide in the 1950s describing vascular system damage and Gilliam on the County General Hospital LA epidemic in 1934 to make the same point, but states that vascular invovlement in ME is not as striking as in IVN

    So at this point it appears as though he might not be equating INV with ME which was consistent with his opening observation but he then states the following which makes it quite clear that he believes they are the same by referencing his NZ trip where he states that it was then that he found that what he called IVN "was the same as ME''

    He states that he believes they are the same disease here:


    Here he uses both the terms CFS and ME in the above paragraph in one single sentence.

    This is extraordinarily confusing. However, what he appears to be saying is that although there are no vascular features mentioned in the CFS criteria, there are indicators of vascular involvement in the historic ME literature. That would be correct.

    However he then makes a distinction between IVN and CFS stating that vascular involvement is more striking in IVN.

    So having said that IVN is the same as ME, he then turns around and distinguishes IVN from CFS, claiming that vascular issues are more striking in IVN. Even so, he still regards IVN as a subset of CFS (ME).

    So from my reading, he seems to be suggesting that INV is the same as ME (which he calls CFS) .

    On the one hand, he makes reference to the historic ME literature and yet, on the other - he seems to approach it as though ME and CFS were one and the same illness.

    So I agree with your general observation, that he appears to be seeing ME as a subset of CFS and possibly INV as a variant of ME within that context.

    But to suggest that IVN is a variant of ME and is a sub set of CFS - is incorrect in my view, for the reasons previously posted (especially the divergent infectious onset periods)

    I think I said I could not recall reading of bruising and painful veins and the other symptoms he described, as being traditionally associated as features of ME.

    I understand that vascular issues are part of ME, in fact that is primarily what is occurring in the brain due to enteroviral activity and inflammation. Hence the hypoperfusion and small bleeds from small vessels.

    What I was in effect trying to say was that the specific symptoms he referred to (bruising and painful veins) I did not view as being commonly reported in epidemics or generally so and therefore, might provide a point of distinction between the condition he calls IVN and ME. He states himself that vascular conditions in IVN is more striking than in ME and that there is scant historical ME literature on this point.

    I do find it remarkable though, that he believes that such painful symptoms can occur at onset of what he describes as IVN, without being noticed especially as he describes it in the following terms : bruises that 'sting' and 'burn', 'swallen veins'' that were ''painful in nature' and veins rupturing that cause ''stinging sensations'' and leave a deep bruise.

    Yes this could be quite possible. It is interesting what you raise here in the context of his discussion of IVN. Muscle pain and fatigue is often commonly discussed, but not throbbing vascular pain. Could it be that patients simple use the term muscle pain to describe this? It is very curious and I despite his claims (and my failure to note such in the historic ME literature), I might take a closer look.

    I agree, that the severely ill do die and have been known to slip into a coma. I do not know though, whether that is reported in the literature in the severely ill ME cases.

    As for extreme drowsiness, I do remember Hyde talking about one ME patient that literally could not keep awake. However, unless mistaken, I had the impression that this was an exceptional case.

    There have been 64 noted symptoms of ME. This does not make it easy for discussion purposes, though primarily in this thread we have been looking at common features so far, that distinguish the illness from CFS or PVFS instead of individual symptoms.

    There will of course be those that crop up that whilst not as common, are still reported in the literature and will be found on that list. When assessing whether an illness like IVN can be distinguished from ME, I look at what are regarded by physicians as key features or commonly recognized features for the purposes of classifying illnesses. This approach is somewhat different from simply recognizing whether symptoms exist in each illness.

    It seemed to me, from reading that article that the author was promoting the vascular element of IVN as a key feature or component of the illness and used it, on one occasion in that article to distinguish it from CFS.

    So I reasoned, if he was promoting it as a key defining feature, then when assessing it against ME, although present, it is not regarded as a key defining feature for the purposes of classification and identifying the disease. So this again, suggested to me that IVN and ME cannot and could not be regarded as the same illness, even though the author asserts otherwise.

    I think his interchanging use of terms is confusing. My interpretation of that sentence is that he is saying that vascular features are not mentioned in the 1988 CDC CFS definition but are alluded to (sparingly as he point out) in historic ME literature.

    With respect to your interpretation of his view point (ME as a subgroup of CFS) although I am uncomfortable with that the term, I understand what you mean, and I have to agree, from my subsequent reading, that this might be correct.

    My personal view is, that those who regard ME as a subset of CFS, do not understand what ME is (as discussed in the historic literature) and or, that the two are distinct and separate illnesses or alternatively, do not wish to make the distinction.

    As we are talking about two distinctive illnesses, it is no more appropriate to medically classify ME as a subset of CFS, as it would be to classify MS there. CFS is a diagnosis of exclusion. Therefore ME must be considered first. The outcome of that consideration will be that you either have ME or you do not. If you have ME, then that would be your diagnosis and there would be no need to consider CFS, let alone consider CFS and determine ME was a sub group of it.

    CFS is a diagnosis of exclusion. Consequently, were you subsequently to learn you had ME, but had been given a diagnosis of CFS (syndrome of unknown cause), then you would no longer be regarded as suffering from a syndrome, called CFS.

    It is impossible and illogical to contend that ME is a subset of CFS.

    I think you might find Tania, that the CDC makes a statement on their web site, which unequivocally states that ME is a completely separate illness with its own distinct medical definition. So I do not think you can contend that the CDC do not fully recognize ME. What they do not and will not recognize (and rightly so) is that CFS as defined by the CDC and CCC is not ME.

    If you go back a few pages, rlc made a post which indicates that the CDC have known this from the inception of the 1988 definition of CFS.

    What they have not done, which might be something for ME advocates to push for is that they have not provided material on their website in relation to ME.

    I understand where you are coming from here, but from my pov and one of the objectives of this thread, is to make things clearer, and to encourage people to learn about/understand and apply the correct terminology, because until we do what makes you think the CDC is going to me motivated to make a change?

    And who will be motivated to investigate those who may have ME but have been left with a CFS diagnosis?

    *citations from Infectious Venulitis Chronic Fatigue Syndrome Myalgic Encephalomyelitis -Erich Rhyll MD from the Committee for Justice and Recognition of Myalgic Encephalomyelitis here:
  14. insearchof

    insearchof Senior Member

    Hi Bob

    I agree....its not a pleasant realisation that this is going on, in an effort to reclaim our health.

    The problem here though Bob, is that the WPI could equally be selecting PVFS patients with CNS dysfunction (G93.3) and not ME patients that would meet the literary criterias we have been discussing.

    Unless I am wrong, I thought from reading your posts on XMRV, that you were of the view that a true replication of the Science paper had not been done and was necessary. I did not think you subscribed to the current view, for example that the Singh study was so close to a replication study, that -near enough is good enough so to speak.

    If that is your view, then surely you understand the need for precision in this area of science as it relates to cohorts - and that would extend to selecting out a specific ME cohort, which has not been done to date.

    Whilst I do believe WPI may have studied some of the Lake Tahoe co hort, I do believe statements on the WPI site do confirm what rlc posted - which was that they were not used for the purposes of the Science study. And whilst it might be true that some persons with CNS dysfunction are within that group - we do not know with any degree of certainty, whether this stemmed from PVFS for example or a misdiagnoses CFS patient with ME.

    This has been the problem ME patients have had to contend with all along - left guessing - whether studies involving a CCC co hort with CNS presentations -might have contained ME patients.

    Why though, should these patients be left wondering?

    It's just not a very scientific approach is it?
  15. Bob


    England (south coast)
    I'm personally in favour of as much scientific research being done as possible, with the most specific diagnostic criteria possible.

    But seeing as we are where we are, I'm pleased that the WPI are doing what they do.
    When I talk about the WPI, I always thinking about their entire body of research that I'm personally aware of, which isn't entirely helpful, because not everyone follows it as closely as I do.

    The unpublished XMRV study that the WPI carried out on UK ME patients was on a self-selected group of fairly average CFS/ME patients, who were not especially picked from a specialist doctor. The unpublished, but released, initial results show that the detection rate for XMRV held up in this group of patients. (I can't remember the exact percentage.)

    This leads me to believe that, if the WPI's XMRV findings are not due to contamination, then XMRV is relevent to the average CFS/ME patients that I personally recognise as having ME.

    If it turns out that the majority of us don't actually have ME, but we all have some other similar immune disorder, then at least the research is being carried out on a large and possibly homogeneous sub-group of CFS/ME patients, which is hopefully better than nothing in this case.

    But yes, I agree that it would be helpful to be as specific as possible with the research, although, politically speaking I don't know if this would be either productive or possible at this time.

    If the WPI had only used an exclusive 'ME' selection criteria, then the CDC and Wessely & Co would have instantly dismissed the research as irrelevant to the CFS population, which in the UK and the USA, is almost everyone! If the WPI used unofficial diagnostic criteria then they would get even more criticism from the establishment than they do now, and the research would have been quickly sidelined, and dismissed. Although White & Co can apparently get away (at least for the time being) with using any old random unofficial criteria for the PACE Trial, the WPI would not be able to.

    I think that the WPI have played a clever game, and they have been very politically astute to devise a clever selection method for their patients. Don't forget that they chose these particular patients because these are the patients who they see every day. It wasn't some dreamt up random selection procedure which selected random patients. They devised the selection procedure in order to fit their patients. If their patients don't have ME, then they have some other serious immune or neurological disorder that needs investigating, but I believe that they have ME.

    Personally, I agree that, in practical terms, the most selective criteria should be used at least for research purposes.
    The major problem is the politics, and the fact that we just don't have an official diagnostic criteria for ME. (At least there's not one in the UK - Do any other countries have an official ME diagnostic criteria?)
  16. *GG*

    *GG* senior member

    Concord, NH
    I believe that Cort/Phoenix Rising website did not support PANDORA letter to some US Gov't agency (I think you can find that letter somewhere on this website). Not all of us, perhaps very few, technically (became) sick during an epidemic. I am not aware of an epidemic when I became ill, it was spring time and it was a rather typical Mono start to my illness.

  17. Tulip

    Tulip Guest

    Of all the severe M.E. patients I have known and read about, I have never heard of someone with M.E. going into a light coma or similar, infact it is quite often the complete opposite. I don't agree that it is an M.E. symptom, but a symptom due to something else going on.
    I also don't agree that you have to be bed bound to be severely ill, people who are mobile also die from M.E., heart failure is common. The death rate for M.E. currently sits at 10% which is a huge number of deaths, I strongly suspect it is more like 20% because a huge number go unrecorded as an M.E. death.
  18. insearchof

    insearchof Senior Member

    Hi Bob
    I agree that the WPI research relates to CFS.

    However, personal observations are not reliable as you know. If that were so, science would be a redundant discipline.

    The trouble with personally recognising something is - that it is subjective observations not based on science.

    ME has been reported to have 64 recognised symptoms that fluctuate in their severity and duration.

    Therefore, at any one time an ME patient on personal observation, might resemble having MS, AIDS, and or any other number of illnesses, yet they do not. Likewise, those you observe - might appear to you -at any point in time -to have ME, when they may have PVFS with CNS dysfunction or a number of other illnesses that resemble ME.


    I realised that.

    I am not criticising the WPI for the cohort they selected. All I am saying is, that the research - whilst important, which I support and find very interesting - is not directly applicable to and or therefore useful for, those with ME. Otherwise I agree with you.

    Well Bob, if that is so - I guess we dont have official diagnostic criterias for any other illness either.
  19. insearchof

    insearchof Senior Member

    Epidemics, ME literature, Changing CFS criteria, CDC, Pandora and other orgs

    Hi GG

    Whether you or very few became ill via an epidemic is not really the point.

    Recognition of the historic ME literature - a lot of which centered around individuals presenting with ME and what was observed in them/their condition - came out of studying epidemics, this is true. However, it was the epidemics that made this illness visible. That in turn, enabled the illness to be fully scrutinized, studied in patients and understood.

    Recognising the historic ME literature means recognising ME as defined there. Due recognition and promotion of this forgotten material, would assist the medical profession today, in diagnosing sporadic cases and sporadic cases, will I believe, be the continuing norm.

    The reason I say that is, - that surveillance and reporting requirements with regard to infectious and communicable diseases has changed over the years and I am not so certain that doctors report suspected outbreaks in the ways they once did, unless their general practices are seeing large numbers of the same illness. Even then, I wonder whether they just write it off to seasonal gastro etc. So many epidemics that perhaps were once seen and reported, especially with regard to ME, will fly under the radar today. That is not to say however, that the epidemics are not taking place.

    Recognition of that literature = recognition of ME and = recognition of what ME is for the purposes of assisting with individual diagnoses.

    However, for literature with respect to a distinct and seperate illness (ME) to be recognised in a CFS document or criteria or any other illness criteria for that matter, should not be expected or promoted in my opinion. You do not see literature on diabetes containing all of the literature relevant to measles do you?

    It is generally understood that the Lake Tahoe co hort was an ME co hort.

    If Pandora understood the distinctions being made in this thread, they might have made a suggestion other than the one they called for in their letter: to change the CFS criteria to also include a criteria for ME.

    The CDC know what ME is. They have known since the lake Tahoe outbreak. However, they appeared to have considered the illness at Lake Tahoe as ME, but believed that it was not. What they believed and had evidence for - upon which to construct a case definition - was evidence of a mono like illlness.

    In the eyes of the CDC and others who understand the distinctions being discussed on this thread, Pandora is asking the CDC this: Please change the criteria of illness A to also include illness Y

    I understand why they are doing that. They are saying to the CDC, ''you got it wrong - now change it''.

    The CDC reply will be: ''We called it as we saw it. We defined it on the basis of the evidence we found at Lake Tahoe at the time.''

    The CDC may have only found evidence of mono at Lake Tahoe - but that is not to say that the evidence for ME did not exist. It did. Hyde diagnosed those at Lake Tahoe as having ME, but I believe it was subsequent to the construction of the definition. Rlc also did a post a few pages back, that makes a strong case to show that the CDC knew what ME was at the time of their investigations/case definition and considered such.

    So there are only two ways around this.

    1. Sue the US government and CDC for negligence and seek a court order for one of more of the following:

    a. that the CFS criteria be set aside AND
    b. that the Nightingale definition of ME be substituted in its place.


    a. maintain the CFS criteria AND
    b. remove guidelines that suggest that standard tests are adequate to get to the bottom of a medical problem that medicine does not have the answer for AND
    c. actively endorse the Nightingale Definition of ME, promote it and train doctors across the globe in its application in a clinical setting.

    Failing that, Pandora and other orgs, will have to accept that the CDC definition of CFS was formed on the basis of evidence found of a mono like illness and that CFS now has a distinct definition that runs alongside the historic ME definition - which the CDC have also acknowledged is a distinct and seperate illness and has a medical definition distinct from CFS.

    In which case, Pandora and other orgs need to push for the just recognition of ME as outlined in the historic literature - independent of ANY CFS criteria, and push for the endorsement, promotion and education/training of doctors around the world on the Nightingale Definition of ME - a definition that amounts to a summary of the historic ME literature, created by an institution that has been solely devoted to the study of ME as historically understood and defined. Whilst they were at the negotiating table, they should also pressure the CDC to remove the restrictive guideline associated with CFS, with respect to testing, which effectively denies patients the right afforded to all other patients - finding possible bio abnormalities and possible underlying causes of their illness missed by physicians. If the CDC was smart, they would accept this and do so quickly, if they wanted to avoid a large class action law suite.

    That just might be a win win solution and an answer to many problems.

    With more doctors knowledgable on what ME is and how to diagnose it - patients who believe they may have ME would be able to seek a diagnosis. Further, future patients would be required to be considered for ME, prior to being given a CFS diagnosis, the later generally being a diagnosis of exclusion.

    As for the Board of PR not supporting the Pandora letter - it may have been that they did not feel comfortable with one or more points raised. I don't know.

    I am not sure of the significance of that point, unless you are suggesting that they do not support and or support the due recognition of historic ME.
  20. Bob


    England (south coast)
    There was a mention of some ME patients being admitted to hospital in a coma, in a paper by Ramsay that I read recently.
    I think that he suggested that it might be due to low blood sugar levels.
    But I've not seen any other mention of patients in comas anywhere yet.

    I know people who sometimes pass out, or faint, but that's entirely different to a coma.

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