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"The Oxford Definition: It's Baaack”

Discussion in 'General ME/CFS News' started by Ember, Dec 22, 2012.

  1. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    Personally i think the definition for ME is very vague which is why its under the cfs umbrella. As august has said we need good research, we need biomarkers etc etc Just using symptoms is to vague, even the best ME definition is mostly symptoms. I dont see anything wrong with putting people into subsets as i think this will improve treatments. Its been mentioned before but like cancer it is put into subsets although the word subsets isnt used, there are many forms of cancer and i think its going to be the same with cfs/me with the common theme being immune dysfunction. Maybe they need to get serious with diagnosing cfs/me and use the nk function test and cd8 t cell function test as apart of a diagnoses, that would weed a few of the patients that have some other illness. We know these immune abnormalities, we should be asking why its not being used??
    taniaaust1 likes this.
  2. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is an etiologically unexplained disorder characterised by irregularities in various aspects of the immunological function. Presently, it is unknown whether these immunological changes remain consistent over time. This study investigates Natural Killer (NK) cell cytotoxic activity, NK cell subsets (CD56brightCD16- and CD56dimCD16+) and cytokines, over the course of a12 month period in patients with CFS/ME.

    Methods

    The participants in the study comprised 65 (47.2+/-11.5 years) CFS/ME participants and 21 (45.2 +/-9.3 years) non-fatigued controls. Flow cytometry protocols were used to assess NK subsets and NK cytotoxic activity at various time points that included baseline (T1), 6 (T2) and 12 months (T3). Cytokine secretions were measured following mitogenic stimulation of peripheral blood mononuclear cells.

    Results

    NK cytotoxic activity was significantly decreased in the CFS/ME patients at T1, T2 and T3 compared to the non-fatigued group. Additionally, in comparison to the non-fatigued controls, the CFS/ME group had significantly lower numbers of CD56brightCD16- NK cells at both T1 and T2. Interestingly, following mitogenic stimulation, cytokine secretion revealed significant increases in IL-10, IFN-gamma and TNF-alpha at T1 in the CFS/ME group. A significant decrease was observed at T2 in the CFS/ME group for IL-10 and IL-17A while at T3, IL-2 was increased in the CFS/ME group in comparison to the non- fatigued controls. Overall cytotoxic activity was significantly decreased at T3 compared to T1 and T2. CD56brightCD16- NK cells were much lower at T2 compared to the T1 and T3. IL-10 and IL-17A secretion was elevated at T2 in comparison to the T1 and T3.

    Conclusion

    These results confirm decreases in immune function in CFS/ME patients, suggesting an increased susceptibility to viral and other infections. Furthermore NK cytotoxic activity may be a suitable biomarker for diagnosing CFS/ME as it was consistently decreased during the course of the 12 months study.

    http://www.mecfsassist.org/1/post/2...reased-immune-function-in-mecfs-patients.html
  3. Ember

    Ember Senior Member

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    The ICC is a more restrictive definition than the Oxford, Reeves or Fukuda definitions, so the ME patient population that it identifies must necessarily be a smaller one. As a patient group, then, we can't all be included in the ME subgroup.
  4. taniaaust1

    taniaaust1 Senior Member

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    They havent dropped CFS they just have made a separation between CFS and ME. Those who dont fit into the ME definition.. remain as CFS.
    Ember and Wildcat like this.
  5. taniaaust1

    taniaaust1 Senior Member

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    Im surprised that the DSM hasnt got an offical Wesselyphobia diagnoses yet in their mental health manual or havent as yet created an Exercisephobia catagory.
    August59 and heapsreal like this.
  6. Nielk

    Nielk

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    I thought that they said that those who don't fit exactly the ME criteria have Atypical ME. I thought that they dropped CFS all together.
  7. In Vitro Infidelium

    In Vitro Infidelium Guest

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    The problem is that smaller doesn't necessarily mean more specific. There is no reason why the gross symptomology used for any of the published case definitions or criteria sets should achieve specificality because none of the gross symptoms used are evidence of specific aetiological processes. The CCC and ICC merely describe random sets within Fukada and Oxford. Reeves has seperate problems and appears to set a random boundary outside of Fukada without obvious justificatio, but in any case it doesn't add to the specificality of the CCC and ICC.
    It's worse than that - variability and relapse/recovery mean that many people would seem to fall in and fall out of the CCC without obvious justification, while the ICC qualifies anyone with post viral illness whilst potentially excluding patients with serious chronic ill health problems common to what most of us understand as M.E/CFS. The CCC was a worthy attempt at more precise definition but hasn't yielded facility in either resarch or diagnosis, and the ICC makes no sense at all.

    IVI
  8. Ember

    Ember Senior Member

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    Atypical ME requires PENE and five (rather than seven) of the remaining criterial symptoms:
    Patients who satisfy the ICC are removed from the broader category of CFS. Those
    who don't remain in the more encompassing CFS classification:
  9. Valentijn

    Valentijn Activity Level: 3

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    The papers I've been reading by Simon Wessely express a similar view, and for similar reasons. To start with, he views ME/CFS as simply being on the extreme end of a continuum of "fatigue". This is a recurring theme, from his earliest work through his latest.

    Then he uses the presumed psychiatric overlap of conditions (especially psychosomatic) to show that differentiating between fatigue and ME/CFS using physical symptoms is meaningless. His reasoning seems to be that since the CDC definition requires patients to have some physical symptoms, it results in selecting many patients who qualify for psychsomatic diagnosis. Of course the CCC/ICC would be even a worse transgressor, in his view.

    Finally he argues that the definition of ME/CFS should not include a minimum amount of required physical symptoms to include a patient, and if anything should have a maximum number of physical symptoms, to exclude patients with too many physical symptoms.

    It's a rather fascinating perspective, until you look at the results of such a division: patients could retain the same diagnostic label (though he would drop "ME" entirely) if they lack physical symptoms, so CFS would exist entirely of relatively simple fatigue (he's not fond of the chronic requirements either).

    But where would patients with physical symptoms go? He does not suggest we be separated into a new category, as some patients or ME advocates might, so the most likely justification for removing us from "his" CFS without a new category would be to put us into an old category - psychosomatic.

    Wessely and his colleagues repeatedly express an unquestioning belief that psychiatric illness is present in about three-quarters of ME patients. These beliefs are based on studies using questionnaires focused at assessing psychiatric problems, and the psychiatric questionnaires being used have a rather large number of questions that involve physical symptoms. The result, of course, is that patients with ME or any other systemic physical illness will be seen as strongly psychosomatic based upon giving typical answers for someone with their illness.

    This would seem to be a deliberate result that Wessely is looking for. To start with, even the anxiety/depression questionnaire used makes certain presumptions about physical and cognitive capabilities, which could easily result in a borderline score for ME patients (interpreted as positive for psychiatric illness by Wessely & co).

    And physical illness can be accounted for even with psychosomatic questionnaires. For starters, the one I took when starting at a "fatigue" clinic included four sections (much like the much briefer General Hospital Questionnaire used by Wessely), but with the caveat that a patient should not be considered psychosomatic when only the somatic section gets a high score - a corresponding high score from one of two of the other categories is also required. This makes more sense (though still doesn't account for depression caused by being chronically ill), because only an idiot would think that a somatic questionnaire is infallible, unless they also think that physical illness does not exist.

    Another way to account for potential physical illness in a psychiatric questionnaire would be to compare ME patients to patients with similar symptoms but with an illness that has been unequivocally established as biological. I believe MS patients are used to that end by some researchers. But the Wessely school prefers comparing ME patients to either healthy controls or patients with muscular disease. Healthy controls do not have constant headaches or pain, etc, of course, hence answer psychosomatic questionnaires rather differently than ME patients. And by choosing controls with purely muscular dysfunction, issues regarding sleep and headaches and such (maybe even pain) are rare enough to earn patients a low psychiatric illness score.

    While a great many researchers do manage to find mood and psychiatric questionnaires that are appropriate for physical disease, and put them into context by comparing them to diseases with known physical causation, Wessely & Co habitually do the opposite. They don't seem particularly unintelligent, so this may very well be a deliberate choice on their part. At any event, relying on this sort of research to presume physical symptoms are not an important part of ME/CFS is beyond ludicrous.
    Wildcat and Tito like this.
  10. medfeb

    medfeb Senior Member

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    IVI - I dont quite understand what you are saying here. As I see it, CCC and ICC are not random sets of criteria within Fukuda or Oxford but a significant tightening up of what are much more random sets of patients. This is especially true of Oxford which only requires 6 months of fatigue and no other criteria and does not exclude primary psychiatric illness - essentially would allow anyone with chronic fatigue.

    On the other hand, the CCC and ICC requires specific symptoms like PEM/PENE. While it is true that PEM/PENE has not been proven to be evidence of a specific etiological process, there is good peer reviewed and objective (not just patient reported) evidence that this represents a pathological process in the body - the work of the Lights showing the physiological reaction to exercise and the work of the Pacific Fatigue Center using CPET (the gold standard for functional capacity evaluation by numerous medical associations) showing the functional impact of PEM/PENE.

    There are plenty of diseases where there is not yet proof of the specific etiology but there is still enough understood about the impact of the disease process in the body to be able to use it as criteria for the disease. In this case, I think the randomness problem is a problem with Oxford and to a lesser but still too significant level with Fukuda that CCC and ME-ICC are trying to solve.

    What am I missing?
    Roy S, SOC, Wildcat and 2 others like this.
  11. Holmsey

    Holmsey Senior Member

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    CF and CFS are not the same, ME, CFS and PVS are, at least if you want to talk about the ICD codings. We don't have a singe 'accepted' test which says you have an illness which matches any of the above illnesses labels, in fact, as is clear from this and other threads there's no concensus on what each means. The closest you have to concensus is the ICD coding, and it doesn't make the distinctions this thread appears too.
  12. Purple

    Purple Bundle of purpliness

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    They may attract the same coding but there is a big difference between a short(ish) term, self-limiting and fully recoverable from post-infectious fatigue state and ME/CFS. This is an important distinction - and one that should be made when appropriate -and it's entirely possible that the short term fatigue state is biologically different from ME/CFS. We need research on this.

    From experience, when I got ill the Dr's attitude was 'it's only fatigue, fatigue means nothing, everyone gets over their fatigue in 6 months at the most'. A decade later, I am crippled by this disease, not able to take care of very basic ADLs and dreaming of being well enough to sit and be pushed in a wheelchair.
    Nielk and Wildcat like this.
  13. alex3619

    alex3619 Senior Member

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    Hi Purple. that is a distinction I make too, and which showed up clearly in the Dubbo studies. Post viral fatigue is common. In the vast majority there are no host of secondary symptoms and it resolves naturally in weeks to months. In around one in ten (though up to 8 in 10 depending on the disease perhaps) this goes on to something more serious. That something is what I think ME is. The biochemical and physiological difference between ME and the more common post viral fatigue would be interesting to research. There is a huge gap in our knowledge. Bye, Alex
  14. user9876

    user9876 Senior Member

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    I wonder if that is why some of the CFS services in the UK think they get a recovery rate of around 25%. Patients are referred to them after 6 months post a virus. Some will just recover, for example, (http://journals.lww.com/co-pediatri...e_syndrome_following_infections_in.99581.aspx) Jason reports 13% meeting CFS critria at 6 months 7% at 12 months and 4% at 24. I think there was another paper recently suggesting similar figures. I was wondering if there were two different processes going on (even if the effects are the same). However, it could be thath there is just an exponential recovery rate but I would want some idea of mechanism to suggest that.

    There is of course a UK paediatrician who promises patients a 97% recovery rate. But she says 'you have been ill too long for it to be CFS, it was CFS but we've cured that it must be a psychological problem brought about by the trauma of being ill'. Then she records the child as being cured of CFS and dumps them on CAMHS saying they have pervasive refusal syndrome. I wonder if doctors are getting confused between two different effects especially without biomarkers or even really good ways to describe symptoms.
  15. alex3619

    alex3619 Senior Member

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    This is the same argument I have raised in another thread. With natural post viral fatigue recovery being confused with ME recovery due to the lax Oxford definition of CFS, it is entirely possible there are some recoveries. This would however be spontaneous, not due to therapy, though in studies like PACE it should be reflected in standard care responses.

    Biomarkers are critical. Once we have those the arguments that dodgy research hides behind can be exposed. More and more papers on biomarker discovery are being released. Next year could prove very interesting.
    user9876 likes this.
  16. In Vitro Infidelium

    In Vitro Infidelium Guest

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    In Vitro Infidelium, post 320186, wrote: The problem is that smaller doesn't necessarily mean more specific. There is no reason why the gross symptomology used for any of the published case definitions or criteria sets should achieve specificality because none of the gross symptoms used are evidence of specific aetiological processes. The CCC and ICC merely describe random sets within Fukada and Oxford. Reeves has seperate problems and appears to set a random boundary outside of Fukada without obvious justification[n], but in any case it doesn't add to the specificality of the CCC and ICC.
    I don’t understand your post –unless you are advancing a naked ad hominem: “anything Wessely writes/says = wrong” ? In any case none of your perambulation through Wessely has relevance to what I wrote beyond the simple point that Wessely does appear to have recognised the “bleedin’ obvious” – which is that without aetiological features there is no way to achieve greater secificality, no matter how much you play around with symptom lists.

    IVI
  17. Valentijn

    Valentijn Activity Level: 3

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    It's the only explanation I've seen for arriving at the same conclusion that you reached. Such a conclusion is quite baffling without an examination of the logic behind it, so it does seem rather relevant, especially as you had included no explanation in your post.
  18. Enid

    Enid Senior Member

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    I really do think that logic (theorising of the jump in many) is not part of ME. We are past that in the understanding of pathological findings now. Let's keep down to earth and the obvious illness still reluctant to be recognised by too many.

    We've got it - immune collapse , let's follow.
  19. In Vitro Infidelium

    In Vitro Infidelium Guest

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    Not sure about missing - I think perhaps you may be confusing 'definitive causation' with 'distinctive aetiological process'. To take MS as an example; while the 'definitive cause' of MS is unknown (indeed there may be more than one form of 'causative agency', viral, genetic etc) - there is a single cardinal aetiological feature that defines the condition, that is 'damage to the myelin sheath' which results from an abnormal autoimmune process'. Identifying MS in the early stages or even in times of relapse may be problematic, but there is no doubt what is meant by Multiple Sclerosis as it affects a large patient population.

    M.E/CFS lacks any (currently) identifiable common aetiological process. The various claimed ‘bio markers’ have yet to show any consistency of presence across large patient populations, let alone provide any definable explanation of relevance to reported symptoms across a large patient population. In fact the most significant aspect of the various biomarker studies is the sheer lack of consistency – things are going on in M.E/CFS patients, but they are different things in different people, and that’s no basis for a case definition or diagnostic criteria set.

    The reality is that Fukada does a reasonable job of grouping together patients suffering from a commonality of symptoms which together indicate the existence of an as yet causally identifiable illness. The NICE guidelines achieve a similar effect. Fukada and NICE are diagnostically reasonable and an are unlikely to be bettered without some significant advance in medical science. Oxford was created (22 years ago !) as a guideline set for research and researchers may continue to see it as having facility.

    Fukada ad NICE certainly produce broad patient populations. The claim for the CCC and ICC is theat more narrowly defined patient populations are achieved which are relevant in terms of underlying pathology (i.e they are aetiologically meaningful). The problems with this proposition are obvious but difficult to explain – I’ll resort to analogy:

    If we take these populations (Fukada and NICE) each to be represented by one hundred glass beads contained on separate two trays, where the beads are single coloured at their centres and each multiply and opaquely coloured at the surface, and the range of centre colours is unlimited but produced randomly) and the surface colouration is limited to ten distinct colours but the number of colours present on any one bead is a random function from one to ten, then we have an effective representation of the statistical conditions achieved by Fukada and NICE. It may be that the surface colours (representative of gross symptoms) are causally related in some unknown fashion to the centre colour (representative of underlying aetiology) of each bead, but as the beads sit on their respective trays we have no means of knowing this (we’d need to bust them open and analyse the data).

    The claim of (supporters of ?) the CCC is that every patient (bead) that falls under the CCC would axiomatically fall within Fukada and NICE (i.e sit on one or both trays) – at least no argument seems to have been made that Fukada and NICE exclude significant numbers of people who would qualify under the CCC. The ICC actually has a different number set than Fukada and NICE because the 6 month qualification period is rejected and the total patient population is therefore potentially many times that in the compass of Fukada and NICE. The effective argument in the case of the CCC is that by finding variation in the surface colours of the beads on the Fukada and NICE ‘trays’ or by some means of sampling below the surface of each bead (yet without ever seeing the centre) a number of beads, amounting to less than one hundred, can be selected and that these beads will all have the same centre colour, and that this centre colour is meaningfully different from all the other potential centre colours. The deficiencies of this approach are hopefully obvious to everyone.

    In the case of the ICC, trying to make any reasonable comparison between it and any other criteria set is near impossible because basically the ICC allows that M.E/CFS is equivalent to any Post Viral Syndrome, so while it may exclude depressive states anyone with flu that’s lasted longer than say, the generally accepted ten days from infection to return to normal function, would fall under the ICC.

    For diagnosis Fukada and NICE are the best we’re likely get until research shows biological characteristics that are demonstrable across large populations. For research Fukada, the CCC, Oxford and NICE may have various roles to play at least until definitive phenomena or comprehensive data requires alternatives.

    IVI
  20. In Vitro Infidelium

    In Vitro Infidelium Guest

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    Er - that's setting the position on it's head. There is no basis for the gross symptomology used in case definitions, diagnostic criteria sets or research criteria sets to have any specificity in terms of relationship to underlying aetiology. It's not for me explain the absence - it's for those who keep claiming that there must aetiological specificity that devolves from gross symptoms, and which in turn means that by tighter definition of symptomology a definiable illness can be arrived at, to actually show why this is the case. Quite simply no one can show that aetiologcally 'Jason's Disease' as defined by the CCC and 'Wessely's Disease' as defined by Fukada are in anyway different to one another, nor that there is any physiological reason to consider that they should be.

    To extend the glass bead analogy I've used above - it's just a silly game of marbles which leads no where. Whether Wessely is or is not playing is irrelevant - it's a dumb game that's had far too many people chasing spheres to useful purpose.

    IVI

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