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

Nielk

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I was always under the impression that











I was always under the impression that PEM is the basic requirement for a true ME/CFS diagnosis.
 
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Hi Angela,

This issue isn't supposed to be the elephant in the room in this thread...
I'd like these issues stated clearly, like you have done so, so we can discuss the whole subject fully, in a supportive and constructive environment.

But personally, I think that the practical issue of separating idiopathic CFS from all cases of neurological ME is not as clear cut as you have indicated, for the following reasons...

I don't know if it is always very easy, in practical terms, to distinguish between mild ME (neurological), and other CFS of an uncertain or psychiatric origin.

Many people consider that they have mild to moderate ME, and that's where the difficulties come in, because some people consider that if you have mild ME, then you don't have ME at all. I think that this might be one of the biggest causes of disharmony in our community.

I believe that we should take the people with mild ME with us, if we propose any changes to the diagnostic criteria to be used clinically or for research. And it seems, from this thread, that this is not such a difficult thing to do, but that we can easily agree on certain changes.

I think that it can sometimes be too easy to get caught up in our differences, when we only have slightly different experiences from each other.

Here's another example of the difficulties of separating CFS from ME: Idiopathic fatigue is considered a psychiatric problem, and not a neurological disease. But a problem that I see with this is that depression can cause severe fatigue, and depression can be 'organic' in origin, rather than psychological in origin. For example, bi-polar depression is widely considered to be 'organic', so doesn't this make it a neuroimmune disease, or very similar? I believe that other forms of depression can have an organic origin as well.
So my point here is that to try to clearly separate ME as a neurological disease from CFS as a psychiatric disease might not always be straightforwards in a practical sense, although I do agree that ME can, and should, be clearly defined as a separate entity.

I'm not trying to be difficult here, by raising these complications... I'm just pointing out that this is a very complex and sensitive area that needs to be sensitively explored.

Personally, I've suffered from depression in my life, and now I've got ME, so I can compare the two, and have no problem distinguishing the two (usually, although it can be confusing at times as they both affect my brain.)
When I used to suffer from what I called 'depression', I was certain (and still am) that it was of biological cause, with an environmental impact on top.

But if I had not experienced severe depression before, and then if went down with mild ME, then would I definitely know the difference?

From first hand experience, and from the experiences of my local ME community who all have fluctuating symptoms, I know that there are different levels of severity of ME. .

I just wanted to point these things out. But having said all of this, we do, on this thread, seem to be in agreement about what minimum changes our community could propose in order to make our lives better.

Insisting on the inclusion of 'post exertional malaise' as a symptom seems to be acceptable to everyone so far, even for clinical use.
And the CCC seem to be acceptable to everyone as a tool to be used for research.

So there seems to be some significant agreement between us all.
Hi Bob,

I completely get the complications here that you've said, especially around severity of illness.

ME and some criteria using CFS show infective or post-infective organic dysfunction similar to other infective diseases. A good use of parsimony would address that. The problem has been the the LACK of parsimony: the tendency of doctors to practice fallacious neo-Freudian psychogenic diagnoses by defualt on illnesses they have problems understanding, and the intention of psychiatrists to claim power and status in mainstream medicine by claiming psychogenic causation in many illnesses, but especially those difficult to diagnose. Frightening gender discrimination, historically and even today, has also had a larger part to play in the social construction of illness experiences than people realise.

You say you believe your depression is different to your 'whatever' (CFS or ME) though? The question is - why? Even with problems with lack of access to knowledge about say, neurological dysfunction, do your symptoms concur with a certain set of criteria, for example? What makes them different to your 'depression' (I'm not asking directly- just making the point, and not using the term 'depression' in quotation marks to be insulting in any way, just to show even this diagnosis can be unsafe).

Psychogenic dismissal is the elephant in the room here, sadly.

If, for example, 'depression' in the absence of distressing life events (let's face it, most depression is caused by distressing life events!) has a neurological cause, then it is a neurological disease. If bipolar/schizophrenia are caused by disturbances in the brain, that makes them neurological diseases, not psychiatric, as it turns out!

But there are many neurological conditions in the absence of mental dysfunction also. Many people have ME/CFS in the absence of 'mental health' problems as such. There are many variances in severity within neurological illnesses also- which, in the absence of the spectre of "it's your disordered mind, love" beliefs, are, in biomedical terms, understandable.

That's before we even address the problem of what is 'mental illness'? Bearing in mind the psychiatrists' tendencies to psychopathologise what are likely normal responses - and in the case of Canadian or Ramsay defined 'ME' normal responses to distressing illness.

The complications are there, especially around illness severity. They need addressing - but in a critically deconstructive way. I think this woudl help address most of the inevitable problems uncovered here. But it's a big job of course.
 

Bob

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I presume that's the paper/criteria that's already out - I mentioned it earlier in the thread: http://forums.phoenixrising.me/show...-s-differences&p=156423&viewfull=1#post156423
Thanks Dolphin...

Oh, so this is this the paper that I'm still waiting for Jason to publish! Doh! :rolleyes:

I'd read that Leonard Jason was still working on an operationalized model of the Canadian Consensus Criteria definition that will allow it to be used for research purposes, and so I didn't think it had already been published.

I haven't read the paper yet, but do you think this is the work that I was referring to? (i.e. "an operationalized model of the Canadian Consensus Criteria definition that will allow it to be used for research purposes.")

I suppose I should print it out and have a look at it... :(
(This might be where I go strangely quiet on the subject!!!) (At the thought of reading the paper!)
 

Dolphin

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Thanks Dolphin...

Oh, so this is this the paper that I'm still waiting for Jason to publish! Doh! :rolleyes:

I'd read that Leonard Jason was still working on an operationalized model of the Canadian Consensus Criteria definition that will allow it to be used for research purposes, and so I didn't think it had already been published.

I haven't read the paper yet, but do you think this is the work that I was referring to? (i.e. "an operationalized model of the Canadian Consensus Criteria definition that will allow it to be used for research purposes.")

I suppose I should print it out and read it... :(
(This might be where I go strangely quiet on the subject!!!)
The short answer is that it is:

-a model of the Canadian Consensus Criteria definition - see title:
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
- designed for research - see term "research criteria" below:

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.
- is talking about "operationalizing" (the phrase "operationally explicit criteria"/similar is used a few times).
 
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I don't think that your opinions on those subjects are helpful for the discussion we are having on this thread.
If you want to limit the terms of what is discussed in a thread it would be helpful if you stated upfront what you consider to be permissable. My response was to this specific paragraph as posted by Sickofcfs:

IF we agree on all the above questions -- which I realize we may well not -- then I suggest that we consider ourselves patients with neuro-immune, or neuro-endocrine-immune illnesses. We might even give ourselves a common name, even if it's not used by the medical authorities, that allow us to work as a group. For example, we might call ourselves, as a group, patients with NEI diseases, or some such.

So ASD, MS, GWS and ME are not neuroimmune diseases? What are they then? I don't really consider it quackery to define those diseases as neuroimmune diseases. And I also don't consider it quackery for the WPI to investigate a range of different neuroimmune diseases, if that's what they want to do. It's not as if they lump the diseases together for clinical purposes.
There isn’t anyway to answer your question because it is posited in relation to a falacy – it’s not possible to give a reasoned answer without disposing of the falacy, and you are insisting that the falacy (neuro-immune disease = something to which an alternative could exist) is not falacious.

To be clear, what I wrote was: There is no clinical description anywhere of such a thing as neuro-immune disease and the term seems exclusive to the WPI who apply it to a whole pick and mix of unrelated conditions in the style of the worst psuedo science quackery. That is, it is stylistically comparable to the numerous quack operations who use scientific language to present a non scientific premise.

What the WPI does is a matter for its Board and its funders, but that’s not the issue I was raising – the issue is what does neuro-immune disease mean ? and the only source for the term is the WPI. What the WPI is claiming about clinical linkage is not clear, but they are classifying M.E within a disease ‘family’ that uses the title neuro-immune disease, and as that term is currently only used by the WPI, the WPI classification has relevance.

IVI
 

insearchof

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For Bob

I have very little insight into Byron Hyde's SPECT scans, but it seems to me that if they were to be widely used and accepted by the ME patient and scientific communities, then the research would need to be successfully replicated by other scientists. To do this, there would need to be very precise definitions about how the research should be carried out, as it would need to be precisely replicated using the description of the methodology. Does anyone know if Byron's SPECT scan research has been successfully replicated and the studies published?
They are not exclusively used by Hyde and I think you will find some very influential names in the CFS arena use and endorse them too - because they represent the best evidence of damage of central nervous system dysfunction. I have seen numbers quoted by others as something like 80% of patients sent return a positive spect.

If you have ever seen one - they give an immediate and vivid picture of a lack of blood circulation due to vascular damage etc. As stated earlier, they are more commonly employed for use in litigation.


Studies:

The only one I have (but am uncertain if there are others - pubmed search?) is this one:

1. Mena, I Study of Ceberal Perfusion by NeuroSpect in Patients with CFS

I think this paper was published in 1991.

Mena is a world leading authority in the field of Nuclear med. That study also refers to others specifically on the technical aspects of SPECTs but unless your a radiologist or a nuclear scientists, I dont think you will get much joy there.
 

insearchof

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Is exercise prior to a SPECT scan necessary to ensure an accurate result?

For Dolphin

Dolphin you raised on the other thread the issue that your friend who was sent off for a spect scan questioned the result becaue they were not told before hand, that exercise could affect the outcome.

I stated that I thought that where a subject underwent exercise before the scan, this would most likely increase circulation and give a better indication of how much flow was getting to the brain and therefore provide confirmation of hyperpofusion or poor blood flow. I also stated my belief, that should a subject be at rest (no blood flow due to little circulation) I would still expect a positive spect - and the condition to be present.

This is what I have found consulting my notes: hypoperfusion is increased (ie lack of blood flow is more evident) after exercise. This was referred to by Mena in the paper I cited above for Bob and which I coincidentally found referred to in another unrelated paper by Goldstein.

I also examined the information you referred me to in Hyde's text book.

For those who don't have access to that - what Dolphin and I were looking at was the display (and commentary) on three sets of Spects taken on a 37 yold patient and interpreted by MENA

SPECT scans take images of the brain in slices and build up a 3 D picture of it.

The images Dolphin and I were examining were taken of the same subject at rest (figures 1-3), post exercise (figures 4-6) and 24 hours post exercise (fig 7-9)

It was a particular type of SPECT scan called an Xeon Spect (just the name of the machine brand I am told) but it is the one Hyde prefers and recommends.



MY COMMENT ON IMAGES and COMMENTARY MADE ON THEM

Dolphin, I note that whilst images 4-9 show what is described as ''a significant decrease in perfusion'' and ''severely decreased brain perfusion ...24 hours after the brain has been stressed by physical exercise'', it is also reported that at rest the subjects scans showed prefusion defects, that became ''aggravated'' with increased activity.

However, these results show that in this patient, there was evidence at rest, of damage that plays a role in hypoperfusion activity. Exercise only seems to show hypoperfusion in action, but there is evidence of damage at rest. Exercise would only show hypoperfusion in action. But if you knew what to look for that would contribute to that ie damage, exercise probably would not be necessary.

The remarks that accompanied those scans said:

"The pathological brain changes demonstrated in 1, 2, and 3 (subject at rest) were exaggerated by normal physical activity''

That suggests to me, that exercise is inconsequential. If pathology is evident, it will show up and will be exaggerated by ''normal' activity.

I also note that they speculate, that positive spect findings in ME patients might be produced as a result of the following also:

* sleep deprivation
* secondary infection (persumably that affects and gets into the brain)
*cognitive, sensory or emotional factors.

ISO
 

Dolphin

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SPECT scan discussion

I just read the following paper which is freely available. I was pleasantly surprised that I believe I understood the vast majority of it so hopefully others would also (if not understand more):

Full free text: http://www.ajronline.org/cgi/reprint/162/4/935
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, 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.
Here's the conclusion:
In conclusion, SPECT showed more intracranial abnonmalities
than MR imaging did in patients with neunologic
problems caused by CFS. Owing to the nonspecific nature of
the radiologic findings in CFS, MR or SPECT may not be of
great clinical utility either as screening tests on as aids in the
differential diagnosis of the condition
, but our preliminary
data suggest that SPECT may be useful as an objective
method for following the effects of therapeutic intervention in
these patients. Further work, including longitudinal studies of
patients with CFS, is necessary to determine the efficacy of
SPECT in this regard.
It briefly mentions the Mena and Villanueva-Meyer study:

Functional imaging techniques have been used infrequently
to study CFS. Using 133-xenon inhalation/regional
cerebral blood flow imaging and 99mTc-HMpAO Mena and
Villanueva-Meyer [9] noted hypoperfusion in the temporal
lobes, but did not report significant differences elsewhere.
9. 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
 

Dolphin

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That looks like a mixed bag of patients- and there were only sixteen of them?!
The sister paper, drawn from the same group using the same criteria (CDC=Holmes) were used in the following free paper http://www.ajronline.org/cgi/reprint/162/4/943 :

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.

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]
Indeed, the findings on SPECT are nonspecific,
and multiple regional perfusion abnormalities also have
been seen in such diverse conditions as systemic lupus
enythematosus [18], cocaine abuse [11 , 19], and multiinfarct
dementia [20]. The SPECT findings in this study therefore
should not be considered to be primarily of diagnostic importance,
but rather as descriptive data that may be helpful in elucidating
the disease processes in each disorder
.
The researchers did hope to develop them but I'm not sure that ever happened:
In summary, this study indicates that SPECT may help in
distinguishing patients with CFS from healthy subjects and
depressed patients. SPECT was not useful in separating
patients with CFS from patients with ADC, but that distinction
usually can be made with other diagnostic technologies;
moreover, the similarity in the appearance on SPECT suggests
the possibility of similar underlying abnormalities in
ADC and CFS. However, given the limitations cited here, we
intend further studies to determine the value of SPECT in
the differentiation of CFS from other encephalopathic conditions.
These will include precise mapping of MR and SPECT
abnormalities, longitudinal studies, correlation of nadiologic
abnormalities with clinical information, and most important,
using objective regional uptake indexes instead of subjective
defect counts to evaluate focal changes on SPECT. These
efforts may help us to establish more accurately the diagnosis
and prognosis in individual cases of CFS, and ultimately
to understand more fully the pathogenesis of the syndrome.
 
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Dolphin - for some reason I cannot access the paper. But the abstract is saying THREE definitions of 'chronic fatigue syndrome were used to select sixteen patients! What were those three?
 

Dolphin

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Dolphin - for some reason I cannot access the paper. But the abstract is saying THREE definitions of 'chronic fatigue syndrome were used to select sixteen patients! What were those three?
The same criteria were used for both papers.

I'm trying to find out what SPECT scan abnormalities there are that might be used as a diagnostic test.
 

Bob

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To everyone who has posted on this thread, especially recently,

Some people seem to have very specific, but different, opinions about how ME is (or should be) defined, and I'm interested in exactly what diagnostic criteria everyone would ideally use for ME. So please could you share your views if you are happy to do so?

Also, would you view the CCC, or similar, as an acceptable temporary compromise, practically speaking, for either clinical or research use, for the CFS/ME community? Or could using the CCC be an acceptable first step towards your ideal situation?

I refer specifically to the CCC because they seem to have quite a wide recognition factor, and seem to be better known than some of the other definitions. So I think they would be the easiest change that could be pushed for immediately (politically speaking, to use for CFS/ME), especially to use in research in the USA and UK.
 
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The same criteria were used for both papers.

I'm trying to find out what SPECT scan abnormalities there are that might be used as a diagnostic test.
All three criteria were used for each paper? What were the three criteria? The reason this is relevant is because they look like a mixed bag at best, meaning the usual problems with findings, or lack of such.
 

insearchof

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Love to contribute, but will have to do so another time. The system has some serious issues. Have tried to alert Adin, without success.
Have left some of the problems I have been having in the nuts and bolts thread but it looks like its taking time to rectify.
 

insearchof

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The spect studies are very interesting

However, it must be pointed out that they relate to a co hort of patients that were selected using CFS definitions, not ME.

Therefore, the conclusions are not surprising, as CFS on any definition used, is so very wide that it catches a number of persons who have other illnesses. For this reason, the ''cause'' of CFS will always remain elusive - there will never be a consistent singular cause when the definition catches such a diverse cohort and as such, there will never be a single tool or aid that will be found to diagnose it.

Doctors in the CFS world report high percentages of abnormal scans, as well as on other neurological and non neurological bio markers, and yet - none of them have been accepted as a diagnostic tool for the purposes of CFS. In the absence of proof of causation, they are not likely to be accepted as such and further, in the lack of a clear homogenous group, they are unlikey to ever find causation for CFS as stated.

What they might find (such as with XMRV) that certain co horts or sub sets within this definition will have certain distinct illnesses, in which a diagnostic tool might be found. Yet, with XMRV I do not believe that that it will ever be accepted as the cause of CFS - only that a large subset within it, have it. I think what will happen is, that persons with a CFS diagnosis will be considered and tested for XMRV and if + you will then be regarded as primarily having a HGRV and treated accordingly. Those who do not, will be left in the remaining classification of CFS. Because CFS by virtue of the way it is defined, is the is the catch all that ''remains thereafter'' group and this is all due to the definition and the fact that the main characteristic of CFS is unremitting fatigue of a specific duration with PEM - which fits a long list of illnesses.

ME is not characterised that way.

Consequently, I do not understand why anyone would want to adhere to a CFS definition (CCC CFS) or any other, for research or clinical purposes.




ME AND SPECT SCANS

There appears, and I may be wrong, some suggestion that SPECT scans and the results of a SPECT scans are the sole diagnostic test/outcome that determines ME. This is not correct in my view.

Spects are only ONE of a number of tools that are successfully used to demonstrate evidence of damage to the central nervous system.

The key feature of ME as *required* by medical literature and existing definitions (by comparing and contrasting med lit in ME with existing CFS definitions) is central nervous system dysfunction. This is a *requirement* in ME but not in CFS (PEM, unremitting fatigue of 6 months - are the key requirements there)

Evidence of CNS dysfunction can and does show up (including evidence of hypoperfusion) using other tools as well.

Neurological tools like SPECT, MRI, computer driven EEGs, PET etc and cognitive testing are not mutually exclusive tests.

Further, all tests - on their introduction into the clinical market place, might meet high levels of specificity and sensitivity for their required uses, will not always return 100% accurate results. No test results are infalible. That is why Hyde and others do not rely exclusively on SPECTs when making an ME diagnosis - it is only one test used to detect CNS dysfunction. It also provides a physican with feedback to determine if a SPECt for example, that was questionable, might require being repeated.

CNS dysfunction does and will appear on other tests.

ALthough Hyde has stated that he will not generally diagnose ME without a positive finding on a spect (but not hard apparently, as most ME patients do return a positive spect based on his years of research) - what you need to understand is, that this does not mean he and other physicians will not do so.

They also consider:

* findings on other tests that show evidence of CNS dysfunction as well and consider the outcome of all tests collectively.

* As I understand it and have read, Hyde will repeat a SPECT scan - especially where the other results and clinical signs and symptoms suggest ME - because - as with any test - there are factors that may, from time to time, return a false finding.

Finally, the thing to remember about Hyde, is that it is his general practice not to confirm a diagnosis of ME without a positive SPECT because his patients are largely those fighting insurers and are involved in litigation where legal evidentiary standards require the highest levels of proof.

So he makes sure he has a water tight case.

His patients are almost exclusively those that are invovled in the litigious process.

Outside of that process however, I am sure that he would not demand a SPECT if there was the same evidence of CNS dysfunction on one or more of the other tests.

The other reasons he prefers SPECT say to an MRI (just for the purposes of illistration as it is a technology most people know about and readily accessible) is probably because:

*it is cheaper than MRI for example
*MRI does not always show ME pathology
*MRIs are nosiy and can cause ME patients distress and a deterioration in health

As for understanding the distinctions between ME and CFS (CCC CFS etc) I suggest you start by reading this: http://www.hfme.org/testingforme.htm



ISO