Diagnostic Criteria - can we resolve our community's differences?

Bob

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Insearchof, I've brought your quote over from the other thread because I think it's more appropriate to discuss it on this thread.

Hi Bob

Many patients believe that using the CCC would be helpful, in a practical sense, for a number of reasons, if used for research for the ME community. One of the reasons is that it is more specific/exclusive than the current official criteria used for CFS in the USA and for CFS/ME in the UK. And so it would mean more homogeneity in research cohorts.
Yes in CFS cohorts I agree.

But that has nothing to do with ME and to suggest for its adoption for the ME community, is with respect, seriously misguided and ill advised and will never be accepted by those who understand the diffferences on the basis of existing fact: the divergent medical definitions which define the respective illnesses.
Thanks insearchof, for sharing your views on these issues. I find your views very interesting and helpful.

First of all, apologies for this enormously long post... It's a subject that I'm very interested in exploring, but I understand if other people don't have the energy or the same interest in it, so I'm not making assumptions that people will be inclined to engage with this.

I think that most of our disagreement about these issues probably comes from the different way we use the terms 'ME' and 'CFS'.
Both the terms can be used in a strictly evidence-based sense; or also a political (official) sense; or a personal sense.
For example, I believe that I suffer from 'ME' and that's how i refer to my illness. But I am officially diagnosed with 'CFS/ME'. And if I lived in the US, then I would probably be officially diagnosed with 'CFS'. I have never been officially diagnosed using the strict definitions of 'ME', but I still refer to my illness as 'ME'.

When I talk about the 'ME community', I'm talking about it in a practical sense, and I not talking about people who purely have an actual 'ME' diagnosis.
From a UK perspective, when I talk about the 'ME community', I'm actually talking about ME patients who only have a 'CFS/ME' diagnosis.
In the UK, a diagnosis of 'ME' is not available, unless, possibly, if you go private. But almost no one goes private in the UK, so there isn't an 'ME community'. So when you talk about an 'ME community', there isn't one in the UK. Not when using official nomenclature.

So when you talk about an 'ME community', based on diagnostic definitions for 'ME', in the strictest scientific sense of the term 'ME', then where is this 'ME community' that you speak of? We don't have one in the UK at all. And I suspect it is a tiny, minute, community in the USA and Canada, only for those who go and see specialists such as Dr Bell or Byron Hyde. So I don't know where you would find an 'ME' community, unless self-diagnosed, or one of the fortunate few patients of Bell's, Hyde's etc.

So if you don't have an ME community, then how can you make changes in the ME community?

The way that I see it is that the disease 'ME' doesn't officially exist at the moment, in a wider practical or political sense, either in the USA or the UK.
Governments are blind to it, society is blind to it, many scientists are blind to it.
Officially speaking, ME only truly exists in the WHO classifications, medical history books, old research papers, and a very very small number of clinicians, with probably just a hundreds of patients between them.

Only 'CFS' and 'CFS/ME' officially exist, in a wider practical sense, in the USA and UK at the moment.

So my opinions are coming from a place of practicality and pragmatism for the wider community who are diagnosed with 'CFS' in the USA, or 'CFS/ME' in the UK.

I believe that making incremental changes to the CFS and CFS/ME diagnosis is more likely to move us towards the ideal situation for ME patients in a shorter time frame, than attempting a make an immediate change to the ideal political situation for ME patients.

I believe that we are more likely to take patients, scientists, researchers, advocacy groups, governments etc. with us, if we advocate for incremental or step changes to the current situation for the CFS diagnosis.

And in the current political climate, almost everyone with 'ME' gets diagnosed with 'CFS' or 'CFS/ME'.

So when I talk about using the CCC as an improvement for the 'ME community', what I actually mean, is that I think it would be an improvement for all those patients who have 'ME' but are currently diagnosed with 'CFS/ME'.


This is why I wanted us all to have this conversation, because every time someone talks about 'ME' or 'CFS', we all mean different things.

You only refer to 'ME' in the very strictest sense, whereas I often use the term 'ME' to cover everyone I know who has a 'CFS/ME' diagnosis in the UK, and a 'CFS' diagnosis in the USA.
If I were to refer to the 'CFS community', then many people would think that I was only referring to people who have idiopathic 'CFS', so I usually refer to it as 'ME'.
I'm now trying to have more clarity and accuracy in my use of nomenclature.


The changes that I am proposing for CFS or CFS/ME definitions are aimed at making the lives of both CFS and ME communities better. I see this happening because I believe that if the CCC, for example, were used for a CFS definition then this would bring benefits to the ME community through more specific criteria being used on a vastly larger ME patient population (i.e. ME patients with a CFS diagnosis) than currently is the case. Most ME patients have a CFS diagnosis in the USA, and all ME patients in the UK have a CFS/ME diagnosis.

I referred to these communities as an 'ME community' because I know that I, and the people I know, have 'ME'. But officially speaking, I should refer to the 'CFS' or 'CFS/ME' community.

So, yes, when I suggest using the CCC, it would apply to the current 'CFS' community in the USA, and the 'CFS/ME' community in the UK, if we are using official nomenclature. Of course, when using the official name ('CFS' community), this would include patients with undiagnosed 'ME'.


I believe in taking a pragmatic approach forwards for our wider community, which will take all the patients, researchers, scientists, governments etc. with us in making incremental changes that would benefit our community.

I acknowledge that you (I'm going to attempt to paraphrase you, so please correct me if I've got your position wrong), believe that nothing except the strictest interpretation of 'ME' is permissible, in a political and wider practical sense, and anything else goes against us.



It could be used as a stepping stone to even even more exclusive/specific diagnostic criteria if that's what patients want.

What it would be Bob, is a stepping stone to greater confusion. Further, it will not doing anything than simply bury ME once again in CFS. I wont be a party to that I am afraid. Nor wiill those that understand the distinctions and issues.

My opinion is that it would be a stepping stone to less confusion than the current political situation, but I agree that it's not an ideal situation.

Yes, I agree that it would continue to bury ME in CFS, but in my opinion it would be a better situation than we have now, in the political sense.

If I truly believed that we could take everyone with us (patients, advocacy groups, scientists, researches, the medical profession, and governments) in one large step to make everything as it should be for ME patients, then I might agree with your approach to this issue.

But I think you are mistaken if you think that would be immediately possible, without incremental changes.

I think that incremental changes are the only realistic way we have of making changes.

I understand what you mean when you say that the CCC should only be applied to the 'CFS community', and not the 'ME community', but then we need to define what the 'CFS community' is. If we define the 'CFS community' as everyone who currently has an official diagnosis of 'CFS', then this would include a lot of 'ME' patients. So in this case, practically speaking, the CCC would also be applied to patients with ME.


I think that I am approaching this issue from a mainly pragmatic and practical perspective, whereas you prefer to approach it from a strictly scientific perspective. As long as we are both clear about exactly what we mean, then I think we agree with each other on the facts, but differ slightly about the way we would expect to implement changes for the CFS, CFS/ME and ME communities.


I believe that most of the disagreements on the forum about this subject arise from mixed and confused use of the terms 'ME' and 'CFS'. for example, you might be clear in your own mind about what you mean by the term 'ME' and 'ME community'. But like I said earlier, your definition of 'ME community' is different to mine. And my definition of 'ME' is anyone in the UK with a 'CFS/ME' diagnosis. I should be more clear about what I mean.
When i talk about the 'ME community', I'm referring to people with 'ME' who mainly have a 'CFS' or 'CFS/ME' diagnosis.
Like I said earlier, I'm going to be more careful with my words now, so this thread has been very useful to teach me that.


So one of the questions that I'm asking on the other thread is if patients are willing to push for a particular political change, if it is a step in the right direction, even if that change isn't perfect
The simple answer Bob, is no. It would not be helpful for ME at all and with the greatest respect to you and those who are trying to move things forward, please consider reading the historical med literature and other documents and make sure you understand the essential points of difference before you throw yourselfs into calling for or doing anything that INVOLVES ME.
Everyone has a different approach to this, and that's why I set up this thread...
For example, the IMEA, are proposing scrapping the term 'CFS' and replacing it with the term 'ME', which I don't disagree with, but then that leads to all sort of arguments about what diagnostic criteria should be used, and what happens to people with CFS who don't meet the new criteria. These things need to be thought about.

And their proposals also lead to the other discussions we've had on this thread, about people with mild ME, or recovered ME. How do they fit into the proposed diagnostic criteria?


No one seems to be having those discussions in our community, except here in this thread.

The damage that has been done to date, is the direct consequence of a mixing terms and a failing on the part of people to appreciate the facts.
I agree.


I and other ME advocates who feel as I do, will not accept a CCC CFS definition for ME any more than we would accept a diabetes definition for the illness and we will not accept mis use/application of the term to any other illness criteria be it CFS or anything else and for this reason, we will not tolerate ME being applied to such a definition.

The simple fact is, that at this juncture we will not settle for anything. We dont need to. The facts are clear and self evident and speak for themselves. They are perfect as they are, and do not require a step in any direction, only promotion.

The area of CFS is however, an entirely different matter. But CFS groups cannot apply ME to CFS anymore than they could legitimately apply MS to it.


ISO
ISO, Would you acknowledge that the scientific situation and the political situation are two entirely different things for people with ME?



Thanks for the discussion ISO. I appreciate that you might not be able to fully respond to this ridiculously long post.

ISO, I do acknowledge and understand all the discussion points that you have made.
 

insearchof

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Hi Bob


If SPECT scans are to be widely used, then there is an immense amount of work that needs to be done with them, and also an immense amount of work using the Nightingale Definition of ME.

And until that research is carried out, however successful/specific/accurate SPECT scans are, they are not going to be used as a diagnostic tool by the wider medical profession or the wider scientific research community.

Wide scale studies of SPECT scans would need to be carried out using a broad selection of ME patients (i.e. 'broad' meaning selected from different geographic areas and from different clinicians.)

To truly test the SPECT scan theory, we would need some double blind studies to be carried out using other clinicians' patients. For example, the WPI's cohort, or Dr Bell's patients, as long as they meet the Nightingale Definition of ME.
Sorry, I've not read through the papers yet so I'm not certain if Hyde has done successful double blind trials, but I've never heard Byron Hyde mention carrying out any blind coded trials. If he had, then I'm sure we would have all heard about it (i.e. what percentage of patients he successfully diagnosed using SPECT scans in a double blind trial.)
Until such trials are carried out and published, and replicated by other researchers, the SPECT scans cannot, and will not, be widely used for diagnosing ME.
Bob

There is a lot of confusion and a general lack of understanding in this thread on ME and the use of SPECT within ME and generally, how medicine operates.

Medicine does not operate in a vacuum. It seldom uses any test to diagnose without reference to other factors. Today, patients may expect and medicine would ideally like, a test that does this, with 100% specificity and sensitivity for that one illness alone - but that is not the reality. Sadly, we live in a world so technologically advanced in comparison to our parents and grand parents, that we believe that this expectation is valid.


Consequently I strongly disagree that an immense amount of work is required to be done using SPECTs as a diagnostic aid in ME. In the context of the medical literature on ME, they are not promoted as a sole definitive test for diagnosing ME at all. In point of fact, ME was diagonsed successfully prior to SPECTs introduction.


I understand though, to someone that does not fully understand the context of the subject matter - it might appear that an immense amount of work might be required, but that is in fact not the case.


Here is the summary I posted on the other thread.


However this aspect of Hydes work, has been taken entirely out of context and set up as the major stumbling block of ME and Hydes definition (which as previously stated is not a definition at all).

As stated in this thread and on the other one:

1. Spect scans are not used as a single diagnostic tool for ME

2. Spect scans are not used exclusively

3. Spect scans are only one of a number of tests used to arrive at the diagnosis of ME

4. XEON SPECT, PET, QEEG, MRI and neuropsych testing are other tools that show damage to the brain and evidence of CNS dysfunction. Some are more useful than
others in certain circumstances. Hyde has discussed this.

5. A diagnosis in ME, as well as other areas of medicine is based on:


(i) Presentation of symptoms
(ii) Identifying key criteria to distinguish one possible illness from another giving rise to possible considerations for a diagnosis
(iii) Adopting tools in an attempt to confirm the considered diagnoses


So whilst it is true Dolphin, that X-rays find things in the body, CAT scan find things in the body but they are pretty useless for diagnosing ME or CFS ....they are equally useless to diagnose anything when used in and of themselves, without recourse to a. patient history of symptoms. b. a physicians knowledge of key distinguishing characteristics of similar illnesses as a point of distinction to narrow down diagnoses c. other testing tool and aids. It seems to me that this is the point that you are not grasping.


6. Spect scans are not part of any historical definition of ME. They are only one of a number of tools used to assist a physican in confirming how accurate an historical medical definition of ME in a clinical setting might be.

Spect / XEON SPECT scans are not a part of any historical definition of ME simply because ME was identified and defined a long time before the introduction of Spect scans. In point of fact a diagnosis of ME was successfully arrived at by physicans well before their introduction. Unfortunately, people forget this and demand a speedy, infallible, 100% specific, exclusive test for an illness. Medicine has never operated this way.


7. Spects are a nuclear medicine 3D imaging device. It is not employed exclusively to detect pathology (in the form of brain lesions/hypoperfusion/vasculitis) in the brain, but are also used to detect tumours, infections, thyroid and other problems with other internal body organs.



8. As with other diagnostic aids in medicine, Spects are not specific as a sole diagnostic tool, for any one illness. The idea that there should be a specific test to diagnose ME is just a nonsense when this is not the case in other areas of medicine. A diagnosis does not take place on aids alone. To suggest that this is why ME is problematic, is misleading



9. Spects are machines and like all medical machinery, the quality of the image is dependent on the operation of the machine, the knowledge of the radiologist in interpreting the scan, the age of the machine and how regularly it is calibrated. Patient movement during the scan, can lead to poor imaging as well.



10. Despite suggestions to the contrary, exercise is not necessary to show pathology in ME. Abnormalities are detectable at rest. Abnormalities give rise to blood flow. After exercise lack of blood flow is more evident, but is not necessary to detect pathology as has been suggested. Clearly shown by SPECTs on patients with ME by MENA and set out in The Clinical and Scientific Basis of Myalgic Encephalomyelitis and CFS Hyde et al



11. Spects also use a radioactive isotope tracer ingested prior to the scan that makes its way into the blood stream -to show blood flow or lack thereof in the brain.



12. Spects are capable of being used in ways to distinguish one vascular disease state from another ie: dementia and Alzheimers disease from others, for instance.



13. The studies you quote were studies using co horts that were selected on the basis of CFS definition(s).

As to why SPECT and MRI also appeared to differ in their sensitivity to changes in symptoms in patients with CFS, it is very hard to say. It is also hard to say with CFS patients in studies like these, what other illnesses the patients may havehad that remain undetected, because we all know how untenably broad those definitions are and how this results in a number of persons that have a number of illnesses. So it is not surprising to see reference to this:

In the second paper, the location of the abnormalities were generally similar in the CFS and depression groups.14.

The items you post are interesting on SPECTs generally and as they relate to CFS patients, but not for the purposes of ME.


14. In so far as pathology appearing and disappearing in CFS I cannot explain that other than to refer back to the point I made at 13.

A study on ME patients to determine whether this takes place, would indeed be interesting because historical medical literature reports that ME patients from epidemics never recovered. It also makes sense when you understand that ME is associated with enteroviral infection. Interestingly, there are parallels between the influences on eneteroviral infections found in ME and XMRV. For example, enteroviruses are difficult to isolate in serology after initial infectious onset and move quickly to other tissue and organs where they remain (ie hidden reservoirs). They are fed with the release of hormones produced via, physical, emotion and intellectual activity. They also have an adverse impact on the immune system. The degree to which repair takes place in the brain would be directly related to the immune systems ability to clean up virus in the brain (and elsewhere). According to enteroviral researchers and physicians like Dr John Chia, because they disperse to the tissues etc, they must be specifically treated if patients are to recover. Therefore, on the basis of historical reports of large numbers of people who contracted ME in the context of epidemics that did not recover; general medical evidence associated with enteroviruses and the work of those in this area, I think it is safe to deduce that specific brain abnormalities in patients with ME, would be detectable by one or more of the tools referred to at some stage during their illness ie flare prior to being treated on antivirals.


15. Hyde has stated that he will not generally make a diagnosis in the absence of a positive SPECT scan. I have read that he has repeated the scan if and when necessary which all good physicians will do where all other evidence (ie test results, symptoms generally as well as those fitting key criteria) may indicates otherwise. He also recommends other scans and whilst PET scans generally can provide better imaging (not specifically with respect to ME), they are less accessible/readily available and more expensive. He has discussed the pro's and cons of the various tests employed in various circumstances. The fact that he has seen more of these tests (SPECT PET MRI QEEG etc) applicable to ME patients than probably any other physican, suggests he has good reasons to recommend SPECT. As for criticisms that this work remains unpublished, as stated elsewhere, I am sure it is not for want of trying - but with 25 years of denialism - as well as its unfortunate association with CFS - it is unlikely to be a popular subject choice with medical journals. Even Judy Mikovitz complains about the problems she has getting her work published and one would think with XMRV being a hot discovery in such numbers in CFS patients the opposite would be true.


16. Hyde also has a practice of patients that are almost exclusively engaged in litigious matters, which is another reason why he would insist on as much evidence of CNS dysfunction, including a positive SPECT before confirming a diagnosis.


Context is always important.
 

Bob

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...the Jason et al (2010) paper:

Jason,L.A., Evans,M., Porter,N., Brown,M., Brown,A., Hunnell,J., Anderson, V., Lerch, A., De Meirleir, K., & Friedberg, F. (2010). The development of a revised Canadian Myalgic Encephalomyelitis-Chronic Fatigue Syndrome case definition. American Journal of Biochemistry and Biotechnology 6 (2): 120-135, 2010 ISSN 1553-3468. Retrieved from:
http://www.scipub.org/fulltext/ajbb/ajbb62120-135.pdf
has different levels.

Meeting research versus clinical criteria: Table 1
provides all the symptoms as specified in the Revised
Canadian ME/CFS case definition. Some meet full
criteria whereas others who are very symptomatic do
not meet full criteria. We argue as we did with the
Pediatric case definition (Jason et al., 2006) that those
that meet full criteria are more homogenous and might
be best used for research purposes and we now classify
these individuals as meeting the Research ME/CFS
criteria. Still, others might have the illness but not meet
one of the required criteria. We classified such
individual as meeting Clinical ME/CFS criteria. These
individuals needed to have six or more months of
fatigue and needed to report symptoms in five out of the
six ME/CFS symptom categories (one of which has to
be post exertional malaise, as it is critical to this case
definition). In addition, for autonomic, neuroendocrine
and immune manifestations, adults must have at least
one symptom in any of these three categories, as
opposed to one symptom from two of the three
categories. We also have a category called Atypical
ME/CFS, which is defined as six or more months of
fatigue, but having two to four ME/CFS symptoms.
There is also a category called ME/CFS-Like, which
involves exhibiting all criteria categories but for a
duration of fewer than 6 months. Further, a person
could be classified as having ME/CFS in remission if
the person had previously been diagnosed with CFS by
a physician but was not currently meeting the Research
ME/CFS Criteria, Clinical ME/CFS criteria, or Atypical
ME/CFS criteria and must have 0 or 1 classic ME/CFS
symptoms.
I've finally got around to reading some of this paper...
I find the categorisations that Jason has proposed, above, quite helpful.
I'm not sure about the 'atypical' category, because it just seems like 'mild' CFS to me, rather than a different kind of 'atypical' CFS.
I've got much more to read.
 

Bob

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Consequently I strongly disagree that an immense amount of work is required to be done using SPECTs as a diagnostic aid in ME. In the context of the medical literature on ME, they are not promoted as a sole definitive test for diagnosing ME at all. In point of fact, ME was diagonsed successfully prior to SPECTs introduction.
Then why is everyone arguing about SPECTS then, if they aren't important?

If not a lot of work medically and scientifically, then definitely a lot of work needs to be done politically.
I don't think that the political situation is going to change until government funded research dollars are pumped into ME research.
I don't know what the situation in Canada is, but the USA and the UK are not going to realistically adopt ME science in the short term.
 

insearchof

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Hi Angela,



You know - careful argument is fair. Preaching at people calling them cowards and ineffectual- it means you don't have a good argument here and have resorted to the haven of the cognitively dissonant - ad hominem.
That was my theory (and not just mine, as I pointed out) of the community as a collective - not directed towards individuals. I was sharing it - I dont think I was preaching, but if you choose to see it as such, and want to sit in the pews - feel free.

I'f I was preaching -when was that a crime? Preaching can also refer to campaigning - which we need a lot more of in my opinion. By the way, given that your quite into analyzing peoples argumentive style etc, 'preaching'' in the way you used it, is fairly denigrating. Another form of shooting the messenger perhaps? But I am not really interested in this sort of discourse, because it is purely deflective.

ISO
 

insearchof

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Bob

Then why is everyone arguing about SPECTS then, if they aren't important?
Finally...thank you.........I asked this question a while ago - on the other thread - I asked Dolphin - why she was going on and on about SPECTS.

It is not that they are not important or useful - but they have been promoted as the sole diagnostic tool that in and of itself, will distinguish ME from CFS or another illness. This is not correct.

I concluded that the reason for this, was due to a lack of understanding and a failure to see them to their proper context in ME and the practice of medicine generally.

People might read a little on ME from one or two articles that Hyde has written but dont go looking at the historical medical literature, or they read a little of Hydes work, without reading more widely on his work, and then they seize on a couple of choice words by Hyde, ie will only define ME with a positive spect - and then incorrectly assume - that this is the sole and definitive diagnostic test for ME etc.

Having said that - Hyde would know though, how well they work to detect evidence of CNS in ME patients - as distinct from other tools and he has probably found them to be more useful. They are also more accessible and cheaper than PET scans apparently. Further, for the purposes of litigation, he is definitely not going to comfirm a diagnosis without all the evidence he can get. So to say he does not confirm a diagnosis of ME without a SPECT - would be understandable in that setting.

If not a lot of work medically and scientifically, then definitely a lot of work needs to be done politically.
Absolutely.....which includes awareness raising on these matters.

ISO

ps:

Its been hard - because of the dual threads and my trying to play catch up - which I am still doing :(
 

insearchof

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Hi Angela


Originally Posted by insearchof
I am sure it is not for want of trying. But when you have 25 odd years of denialism, how many journals do you know would want to publish on ME?

Maybe he and Judy Mikovitz could share their frustration ''over a cold one'', as we say here.


I get the problem with the issue of publishing in a culture of denialism, certainly. However, it would nevertheless help if Hyde published in a peer reviewed journal. It would be interesting to know if he has tried. Mikovits has published, of course.

In the meantime- we have to work with what we have available to us. Finding CC cohorts that can be differentiated from the 'Oxford' cohorts to research should be a priority for all scientists working on ME or ME/CFS, and highlighting the flaws in Oxford cohort research and its failure to identify ME could be written and submitted for peer review also. Sadly, we just don't know if this is being done.
Mikovitz has because of the fact that it was a new finding. Its hot and topical. ME is not, as you well know.

I may be mistaken, but I was under the impression Hyde had tried. Why not write to him and ask him and/or encourage him to do so - if this is usch an issue for you?

In the meantime, we can work with what we have - agreed: both CFS definitions for CFS research and ME definition in existing literature, for ME research.

ISO
 

insearchof

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Hi Dolphin


Originally Posted by insearchof

Originally Posted by Dolphin
Also, where is the evidence that this or other imaging is so good? Lots of things can sound good in theory but are not so good in practice: that is one of the reasons one does biological research, to test out hypotheses.
Maybe you should ask the FDA who regulates the introduction of the machines before they are put out onto the market.

Spect machines investigate the operation of the brain and CNS dysfunction. They have done this successfully for at a long time. Like a lot of tests and machines (they need to be calibrated regularly, and used in the correct fashion) they are not infalible. IF your searching for a test in medicine in relation to ME CFS or any other area that is 100% reliable 100% of the time - good luck with that.
Well it's the Nightingale definition which mentions that he won't diagnose ME without a positive SPECT scan.

I don't know if your rhetoric above convinces you; it doesn't convince me. The FDA didn't approve the machines as something that diagnoses M.E. for example or finds the CNS dysfunction posited to be in M.E.

What convinces scientists, etc. is published research not mentions of authority, whether they be Dr. Hyde, the FDA, etc.
Dolphin please read my posts to you previously, including the one on the other thread which is posted also at Bob at post 142 above.

Beyond that Dolphin, I cannot help you with your lack of comprehension on the matter I am afraid.

ISO
 

insearchof

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Hi Dolphin

As I stated on the other thread, it seems your friend was disappointed with their spect result. Did it show CNS dysfunction? Did Hyde confirm a diagnosis of ME?

And for someone who values scientific evidence, you are placing a lot of stock in a hearsay report of ONE patient.
My contact was unhappy with lots of aspects of their dealings with Dr. Hyde. I will see try to see what they are happy for me to say. Just to repeat again as I said on the other thread, it wasn't me - I'm not able to travel to Canada or anywhere e.g. my granny died this week in my city and I didn't go to any of the events.

As I said before, I don't need to depend just on what this person said: it's main value has been to prompt me to look again at some of the things he says. And a lot of questions remain unanswered. Published data would be a huge help. He has had been in the field since I think it is 1984. He has been closely associated with the Nightinagle Research Foundation for the past 20 odd years - it's almost sole purpose in the last 15 (?) years seems to be his activities. He has had plenty of time to publish data in peer-reviewed publications. That as I say is much more likely not just to convince me but more influential people in the medical field like the people who pay for tests and treatments (government-type agencies (NHS, NICE, etc.), insurance companies, etc).

Some people (e.g. those who have used him for insurance company cases) may not like him challenged. But so much of the ME vs CFS debate seems to revolve about what he says.

I am only interested in their diagnosis, not their personal views of Hyde.

Some people..... may not like him challenged

No Dolphin, most people do not mind a discussion of his work in its proper context and with someone who actually has knowledge about it. What people dont like is unnecessary personal attacks on the man himself.

For example, how is the following even relevant to the science on ME, Hyde's scientific work on ME or our discussions on this thread?

http://grubstreet.ca/articles/interviews/byronmhyde.htm


GS What are your hopes for the Nightingale Foundation?

BH Id love to raise $1.2 million dollars. The British government has asked me to come to England. It promises 15 million pounds to set up a foundation, such as I have in Canada, to examine the ME patients, in England.

I told them that number one, I didnt trust governments to come across with money or hire a staff and set up a foundation. Ive at least two university students whove offered to house me, but I thought, if I give up my practice here, I cant afford to wait for two years for the money to come or not.

If I had $1.2 million pounds or dollars, I could not only set up the foundation, in the UK until we did get funding. That amount of money would also allow me to come back to Canada and set up at the university here as well to also properly research these people.

[..]

** This is a verbatim transcript of a taped interview, given by Dr. Hyde, on 8 June 2008, and vetted by Dr. Hyde, on 27 June 2008.
You then make reference to the hero worshiping of Hyde by some - again, how is this relevant to the science we are discussing? In any event here is my reply - which I posted in response to this made on the other thread:

Hi Dolphin -

Perhaps I am a little more cognitively challenged today, but I fail to see the relevance of how that post establishes poetic licence or anything else really, other than perhaps that Byron did not have 1.2 million dollars of private savings to help him set up the foundation, relocate and negotiate a transitional period to keep the doors of the foundation open until government funding come through.

Could you please explain this further, because right now its looking like another thinly veiled attempt at a character assassination of one of very few, ME experts.

For those of you unware, Dolphin has pointed out on the other thread - that he/she has problems with what he/she refers to as hero worship that he/she sees being accorded to Hyde.

I have already stated elsewhere, and will repeat -that I did my own extensive reading and research of historical ME literature. I did not simply accept Hydes writings, nor did others I know.

It seems to me, that when you jump into this topic with little or no knowledge, there is an obvious inability to hold a discussion with those who have. What happens is, that little bits of knowledge are taken out of context and general ignorance does not allow for a fuller discussion. It is understandable that people who lack this knowledge and or are unable to appreciate it in a contextual setting, would attempt to hijack the focus by attacking the credibility of leading authorities in the field.

I do not mind an examination of scientific contributions by scientists this should be done, but with a focus on their work and within context.

However, there is no room for grubby suggestion, speculation or inferences or personal attacks -associated with such people - who, it pays to remember, know a hell of alot more than any one of us.

Dolphin, you then go on to say this:


Part of what I have been trying to do is to prompt others to put pressure on him to publish more.
I read quite a bit of the medical literature in the area, submitted letters, dealt with health agencies, seen how NICE works, etc. It's published peer-reviewed data that will make the difference. One doesn't get too far quoting other sorts of text

Heres an idea, instead of you trying to prompt others to put pressure on Hyde to publish - (even though there is already 50 years worth of scientific published peer reviewed literature that already exists on the subject that you could use) why not approach Hyde yourself - if it is so important?
 

insearchof

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Hi Bob
Originally Posted by insearchof

The HIV/AIDS groups looked fear straight in the eye and said -there is no other path. They fought, demanded and acheived. 25 years on, and despite the appearance of WPI, the CFS community is still allowing fear and immediate self interest -to get the better of them. They point the finger at the ME crowd alleging that they are selfish - that if ME is introduced, where will it leave people who do not fit into ME? But the fact of the matter is, many of those who are fighting for the due recognition for ME,do not have an ME diagnosis but recognise that they may have had one, had the truth not been lost. They understand the injustice and the suffering and that this should never have happened. They understand the need for truth and how that plays a part in the greater good - irrespective of what that might cost them personally.


But do you not see the fundamental differences between the ME/CFS communities and the HIV community?

HIV patients were dying quickly, and then they found a virus.
We die slowly, and they haven't yet confirmed the virus.
That makes so much difference to what we can achieve.
People with ME/CFS have been fighting for years for recognition and validation, but we are constantly hitting brick walls. All of us are constantly hitting brick walls, whenever we do campaigning of advocacy (which we do a heck of a lot of, between us all).
If/when XMRV is confirmed then that instantly changes everything, for all of us, and then these discussions will be redundant.

I know that this thread has a lot of information in it and there is a lot going on - its hard for me to keep up with, so I imagine that it must be more so for you.

I did address that point Bob in the post from which you refer (#122 here: http://forums.phoenixrising.me/showthread.php?10017-Diagnostic-Criteria-can-we-resolve-our-community-s-differences/page13


As for XMRV making the discussions redundant as well as my theory - I think you might find otherwise.

Not everyone in the community wants to see XMRV being confirmed Bob. As I mentioned, whilst some org's across the world have issued statements on the matter, others have remained mute and some publicly stated that it would be a mistake for their members to engage in politically lobbying on the matter!

There are those within the community and the org's - that do not like the association of XMRV to HIV/AIDS.

The moment it is confirmed however, the org's and all those who are fearful of this state of affairs - are going to be forced to deal with it.

Not all persons will receive a +XMRV/MLV diagnosis. Lombardi et al test was based on the CCC CFS criteria and those tested were amongst the sickest of CFS patients. Given this, it may well transpire that persons with this positive test result will be regarded as having a HGRV and will no longer qualify as a CFS patient -remember - CFS is a syndrome - a syndrome is a collection of symptoms the cause of which remains unknown. Once the cause of most of your symptoms are identified - problem solved - and you are treated for that illness accordingly. However, the percentage of those from the overall community - that test positive, might be a relatively small number. It is hard to say, but it is a possibility.

Alternatively, if XMRV is found to be the cause of CCC CFS - then those who have a CCC CFS diagnosis - and XMRV is found to cause CCC CFS - then it might transpire, that CCC CFS disappears, with CCC CFS simply being recognised as the end product of XMRV ie CFS is to XMRV what AIDS is to HIV. But that would require proof of causation - and that wont be without its problems because of the breadth of the definition.

If CFS survives as a criteria, then those who do not test positive, will remain within the CFS criteria. And so for these people, the issues, and these discussions will remain alive.
 

Dolphin

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I think we are only arguing about the practicalities, in a wider sense, of using SPECT scans and the Nightingale Definitions, for the wider CFS-diagnosed and CFS/ME-diagnosed communities (including ME patients).
The validity of SPECT scans can only be confirmed, proven and validated by further and wider research. So I can't see that there's much point in us arguing about that..
Good point

I think we would all like to see Byron Hyde's work rolled out to a wider research field, with millions of dollars pumped into it.
The issue is whether this is going to happen, in reality, before other smaller changes are made to the fields of CFS and ME research.
So I think we are arguing about practicalities, more than anything else, which is related to how much Byron Hyde's research has been replicated and validated, on a wider scale.
It shouldn't be forgotten that Byron Hyde has published very very little in peer reviewed journals. Replication suggests to me it has been published before.
 

Dolphin

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Bob said:
But my feeling is that Byron Hyde is a local clinician, local to Canada, without a wide scientific, medical or patient following
Hi Bob

I think you will find that he has a wider following in both the medical/scientific field and patient community that you readily appreciate. Drop Prof Hooper in your country an email and he should be able to enlighten you more.

When he is not seeing patients (across the world), he is writing and lecturing - across the world. He was in Australia, only six months ago delivering addresses on ME and CFS to both medical and lay audiences.

My underlying belief as to why he does not have a wider following in the patient community is as follows:


a. the lack of knowledge on ME and the distinction. This is diminishing thanks to the work of HFME

b. the continued use of a descriptive term ME/CFS that has no factual basis in medicine and only continues to hide the distinctions between ME and CFS in plain sight.

c. a refusal for CFS advocates to do the required research

d. and or having done the research and understood it, fail to promote the facts and truth, due to what I call my fear theory - (previously posted)

ISO
Whatever the level of Byron Hyde's influence, I think he would have a much bigger influence if he published in peer reviewed journals more. As Angela, myself and probably others in this thread have said, one can't get that far quoting what individual doctors said in many situations - one is expected to reference published research.
 

insearchof

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As stated on the other thread, publication of Hydes work will not add - in any significant way - to our understanding of what ME is and how to diagnose it.

His studies on SPECT might provide interesting reading but that is all.

Further as stated, he has been busy seeing patients across the world, lecturing/raising awareness, writing, consulting to governments, running the Nightingale Foundation, raising funding - pretty much on his own in the last few years. Mikovitz has been a busy woman but has not had to juggle half these things on her own. People expect him to publish and continue to do all these things - but whilst your supporting the WPI, how many of you are actively supporting the Nightingale Foundation? Those who hold these expectations - are you doing so or are you simply content to hold these expectations and criticize?


ISO
 

Dolphin

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As stated on the other thread, publication of Hydes work will not add - in any significant way - to our understanding of what ME is and how to diagnose it.

His studies on SPECT might provide interesting reading but that is all.
I find this a strange statement to make.

At the moment, it is hard to refer to much of what he says as it hasn't been published.
And in particular, how specifically SPECT scans may be used and how accurate they are can aid clinicians, health systems, etc.

Medicine has changed from decades ago. Expert statement has a lower value and if the experts are no longer alive to make their case in a discussion, it will likely have lower value again unless what they found has been published or it promted others to publish research along similar lines.
 

Dolphin

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Around a week ago, I asked specific questions about the SPECT differences found in M.E. (what thresholds, etc.) - sickofCFS asked a more general question along the same lines.
I don't believe either of us have received a specific answer to this question.

I have had various things on but I have now looked at four SPECT scan
papers:

Schwartz RB, Garada BM, Komaroff AL, Tice HM, Gleit M, Jolesz FA, Holman BL.
Detection of intracranial abnormalities in patients with chronic fatigue
syndrome: comparison of MR imaging and SPECT. AJR Am J Roentgenol. 1994 Apr;162(4):935-41.
Schwartz RB, Komaroff AL, Garada BM, Gleit M, Doolittle TH, Bates DW, Vasile RG, Holman BL. SPECT imaging of the brain: comparison of findings in patients with chronic fatigue syndrome, AIDS dementia complex, and major unipolar depression. AJR Am J Roentgenol. 1994 Apr;162(4):943-51.
Mena I, Villanueva-Meyer J. Study of cerebral perfusion by NeuroSPECT in patients with chronic fatigue syndrome. In: Hyde BM, Goldstein J, Levine P. eds. The clinical and scientific basis of myalgic encephalomyelitis/chronic fatigue syndrome. Ottawa: Nightingale Research Foundation, 1992:432-439
Costa DC, Tannock C, Brostoff J. Brainstem perfusion is impaired in chronic fatigue syndrome. QJM. 1995 Nov;88(11):767-73.
-----
The thing that comes out is that different findings were found in different studies. It is not clear how contradictory they might be. Also, in the second Schwartz paper, there were a lot of similarities between the CFS patients and the depressed patients. In the Costa study, the average difference in the brain stems when one excluded those patients who also had depression (as well as patients who had other psychiatric disorders).

As I said, average differences do not necessarily translate to differences at an individual level.
For example, in Mena & Villanueva-Meyer, of the 6 regions assessed, there was only a statistically significant difference in the Right temporal region
59.3 +/-14.1 vs 69.2 +/- 3.2. This means that the CFS patients are only 0.7SD away from the mean of the healthy controls i.e. a reasonable percentage are likely to have similar scores to healthy controls.

So it is still unclear to me which tests are supposed to be used faced with an individual patient (e.g. Schwartz counted deficits while Costa and Mena measured perfusion).
It is certainly unclear to me how good these studies would be for everyone (i.e. the sensitivity and specificity, the "bread and butter" of tests).
As Bob have said, more research needs to be published in the area.



AJR Am J Roentgenol. 1994 Apr;162(4):935-41.

Detection of intracranial abnormalities in patients with chronic fatigue
syndrome: comparison of MR imaging and SPECT.
Schwartz RB, Garada BM, Komaroff AL, Tice HM, Gleit M, Jolesz FA, Holman BL.

Department of Radiology, Brigham and Women's Hospital, Boston, MA 02115.

Abstract
OBJECTIVE: Chronic fatigue syndrome is a recently characterized condition of unknown origin that is manifested by fatigue, flulike complaints, and neurologic signs and symptoms, including persistent headache, impaired cognitive abilities, mood disorders, and sensorimotor disturbances. This syndrome can be difficult to diagnose clinically or by standard neuroradiologic tests. We performed MR imaging and single-photon emission computed tomography (SPECT) in patients with chronic fatigue syndrome to compare the usefulness of functional and anatomic imaging in the detection of intracranial abnormalities.

SUBJECTS AND METHODS: Sixteen patients who fulfilled the Centers for Disease Control, British, and/or Australian criteria for chronic fatigue syndrome had MR and SPECT examinations within a 10-week period. Axial MR and SPECT scans were analyzed as to the number and location of focal abnormalities by using analysis of variance with the Student-Newman-Keuls option. MR imaging findings in patients with chronic fatigue syndrome were compared with those in 15 age-matched control subjects, and SPECT findings in the patients with chronic fatigue syndrome were compared with those in 14 age-matched control subjects by using Fisher's exact test. The findings on MR and SPECT scans in the same patients were compared by using the Wilcoxon matched-pairs signed-ranks test.

RESULTS: MR abnormalities consisted of foci of T2-bright signal in the periventricular and subcortical white matter and in the centrum semiovale; there were 2.06 foci per patient, vs 0.80 foci per control subject. MR abnormalities were present in eight (50%) of 16 patients, compared with three (20%) of 15 age-matched control subjects. Neither of these differences reached significance, although the power of the study to detect differences between groups was small. Patients with chronic fatigue syndrome had significantly more defects throughout the cerebral cortex on SPECT scans than did normal subjects (7.31 vs 0.43 defects per subject, p < .001). SPECT abnormalities were present in 13 (81%) of 16 patients, vs three (21%) of 14 control subjects (p < .01). SPECT scans showed significantly more abnormalities than did MR scans in patients with chronic fatigue syndrome (p < .025). In the few patients who had repeat SPECT and MR studies, the number of SPECT abnormalities appeared to correlate with clinical status, whereas MR changes were irreversible.

CONCLUSION: SPECT abnormalities occur more frequently and in greater numbers than MR abnormalities do in patients with chronic fatigue syndrome. SPECT may prove to be useful in following the clinical progress of patients with this syndrome. PMID: 8141020 [PubMed - indexed for MEDLINE].
AJR Am J Roentgenol. 1994 Apr;162(4):943-51.

SPECT imaging of the brain: comparison of findings in patients with chronic fatigue syndrome, AIDS dementia complex, and major unipolar depression.
Schwartz RB, Komaroff AL, Garada BM, Gleit M, Doolittle TH, Bates DW, Vasile RG, Holman BL.

Department of Radiology, Brigham and Women's Hospital, Boston, MA 02215.

Abstract
OBJECTIVE: Chronic fatigue syndrome is an illness of unknown origin that begins abruptly with a flulike state and has symptoms suggesting both a chronic viral encephalitis and an affective disorder. We compared single-photon emission computed tomography (SPECT) scans of patients with chronic fatigue syndrome with those of patients with AIDS dementia complex and unipolar depression.

SUBJECTS AND METHODS: We used 99mTc-hexamethylpropyleneamine oxime to examine 45 patients with chronic fatigue syndrome, 27 patients with AIDS dementia complex, and 14 patients with major unipolar depression. Scans of
38 healthy persons were used as controls. Comparison of regional defects between groups, as well as midcerebral uptake indexes (an objective measure of global radionuclide uptake), was performed by using analysis of variance with the Student-Newman-Keuls option. Correlation between the number of regional defects and the midcerebral uptake index was determined by using the Spearman rank-correlation test.

RESULTS: Patients with AIDS dementia complex had the largest number of defects (9.15 per patient) and healthy patients had the fewest defects (1.66 per patient). Patients with chronic fatigue syndrome and depression had similar numbers of defects per patient (6.53 and 6.43, respectively). In all groups, defects were located predominantly in the frontal and temporal lobes. The midcerebral uptake index was found to be significantly lower (p <
.002) in the patients with chronic fatigue syndrome (.667) and patients with AIDS dementia complex (.650) than in patients with major depression (.731) or healthy control subjects (.716). Also, a significant negative correlation was found between the number of defects and midcerebral uptake index in patients with chronic fatigue syndrome and AIDS dementia complex, but not in depressed patients or control subjects.

CONCLUSION: These findings are consistent with the hypothesis that chronic fatigue syndrome may be due to a chronic viral encephalitis; clinical similarities between chronic fatigue syndrome and depression may be due to a similar distribution and number of defects in the two disorders.

PMID: 8141022 [PubMed - indexed for MEDLINE]
Brainstem perfusion is impaired in chronic fatigue syndrome.

QJM. 1995 Nov;88(11):767-73.

Costa DC, Tannock C, Brostoff J.

Department of Psychiatry, UCL Medical School, London, UK.

Comment in:

QJM. 1996 Feb;89(2):163-4.

Abstract
We looked for brain perfusion abnormalities in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). An initial pilot study revealed widespread reduction of regional brain perfusion in 24 ME/CFS patients, compared with 24 normal volunteers. Hypoperfusion of the brainstem
(0.72 +/- 0.05 vs. 0.80 +/- 0.04, p < 0.0001) was marked and constant. We then tested whether perfusion to the brainstem in ME/CFS patients differs from that in normals, patients with major depression, and others with epilepsy. Data from a total of 146 subjects were included in the present
study: 40 normal volunteers, 67 patients with ME/CFS (24 in the pilot study,
16 with no psychiatric disorders, 13 with ME/CFS and depression, 14 with ME/CFS and other psychiatric disorders), 10 epileptics, 20 young depressed patients and 9 elderly depressed individuals. Brain perfusion ratios were calculated using 99Tcm-hexamethylpropylene amine oxime (99Tcm-HMPAO) and single-photon emission tomography (SPET) with a dedicated three-detector gamma camera computer/system (GE Neurocam). Brain-stem hypoperfusion was confirmed in all ME/CFS patients. Furthermore, the 16 ME/CFS patients with no psychiatric disorders and the initial 24 patients in the pilot study showed significantly lower brainstem perfusion (0.71 +/- 0.03) than did depressed patients (0.77 +/- 0.03; ANOVA, p < 0.0001). Patients with ME/CFS have a generalized reduction of brain perfusion, with a particular pattern of hypoperfusion of the brainstem.

PMID: 8542261 [PubMed - indexed for MEDLINE]
 

insearchof

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Dolphin


I have answered your question on both threads now re spect scans......maybe when you catch up in your reading ie posts I referred to above the penny might drop......and if it does not, I am afraid I can't assist you in aiding your comprehension of the subject matter on SPECTS any further....other than to say....it might be a good idea to start researching the history of ME and read widely. You really can't be expected to run before you can walk. Nothing will be clear to you unless and until you do this.


ISO
 

PhoenixDown

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My second point is about SPECT scans, which were actually brought up earlier in the thread (edit: I meant to talk about that but called them PET scans instead /edit)... the problem with using SPECT for positive diagnosis is that some patients have positive SPECT some, but not all, of the time. They do not have positive SPECT once and then not again (as we might expect if it was from an acute infection that then cleared and did not constitute a further problem), but recurrently. Does that patient have ME, then recover, then get ME again? I think not.
It would none the less be a better state of affairs to sub type these illnesses based such scans, until light is shined on more comprehensive evidence. For one it would help change attitudes toward these illnesses which would have a great positive impact on patients, in some cases preventing permanent or long term damage that arises from ignorant attitudes.

Edit: shone/shined/whatever
 

WillowJ

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It would none the less be a better state of affairs to sub type these illnesses based such scans, until light is shined on more comprehensive evidence. For one it would help change attitudes toward these illnesses which would have a great positive impact on patients, in some cases preventing permanent or long term damage that arises from ignorant attitudes.

Edit: shone/shined/whatever
of course. I'm in favor of using all the tests which have been shown to demonstrate pathology in any of our patients.

Additionally, any way we can stratify/subgroup based on robust evidence is good with me.

ETA: I'm not actually aware of any robust evidence for anything which we can use to definitely say we know this ME patient to be qualitatively different from that one