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Research: Diagnostic classification of ME, CFS and Chronic Fatigue

Ember

Senior Member
Messages
2,115
I guess I am concerned that we head increasingly for a situation where various sub-categories are created in advance of any objective testing that definitely identifies cohorts of patients and without any specific treatment to offer said patients.
Some members of the Guideline Development Group, who apparently shared your concerns, weren't prepared to follow the WHO classification for ME. As a result, the NICE Guidelines followed instead the CMO 2002 recommendation “that the composite term CFS/ME is used and that it is considered as one condition or a spectrum of disease.”

Here's a background quotation:
The World Health Organization (WHO) classifies CFS/ME as a
neurological illness (G93.3), and some members of the Guideline Development
Group (GDG) felt that, until research further identifies its aetiology and
pathogenesis, the guideline should recognise this classification. Others felt that
to do so did not reflect the nature of the illness, and risked restricting research
into the causes, mechanisms and future treatments for CFS/ME.
 

Guido den Broeder

Senior Member
Messages
278
Location
Rotterdam, The Netherlands
PEM is still just a symptom, not a disease by itself.

The name ME was given because they found CNS inflammation. By definition, without the CNS inflammation, it is not ME.

Note, however, that there are many more diseases with CNS inflammation, and also many more diseases with PEM as a main symptom. Not all CNS inflammation is ME, and not all PEM is ME.

ME is also postviral, causes muscle pain, and involves the cardiovascular system. That narrows it down to a single disease entity.
 

Guido den Broeder

Senior Member
Messages
278
Location
Rotterdam, The Netherlands
Hi free at last, the 4-7 day incubation period for ME is known, because previous ME epidemics before the invention of CFS were very well studied and a lot of the major ones happened in hospitals, where they were able to track the length of time from a none infected person coming in contact with an infected one and then getting sick, this was about 4-7 days and this finding was recorded in many epidemics.

It is a very overlooked, but extremely important finding, because it means that viruses that have a longer incubation period like EBV, which has an incubation period of 40 days cannot possibly be the cause of ME, it is because of his knowledge of what MEs incubation period is, that Dr Hyde was immediately able to say that XMRV could not possibly be the cause of ME, because all Retroviruses have long incubation periods, see page 7 http://www.nightingale.ca/documents/GoteborgConference.pdf

Unfortunately almost all researchers into infectious causes of ME have ignored the old research into ME and have wasted fortunes investigating lots of different viruses like EBV, HHV6 CMV etc as possible causes of ME, when all of these viruses have long incubation periods which means it is scientifically impossible for them to be the cause of ME.

A combination of factors, like a sleeper and a trigger, might be necessary to induce ME. The trigger (the enterovirus) will determine the length of the incubation period, while the sleeper (the herpes virus) may have been present for quite some time. This is the model that best fits the data, IMHO.
 

Guido den Broeder

Senior Member
Messages
278
Location
Rotterdam, The Netherlands
The anaerobic threshold is indeed low in ME. This is the main cause of muscle pain.
I'd say that PEM is first of all caused by ATP/ADP depletion. A weight increase can be a consequence (rather than a cause), because your metabolism may respond by hoarding fat. Taking carnitine may counter that in part, btw. But other patients lose weight.

None of this is unique. You can for instance be born with a mitochondrial defect.
 

Ember

Senior Member
Messages
2,115
I'd say that PEM is first of all caused by ATP/ADP depletion.
Thanks. I'm interested in the underlying pathophysiology of PENE and whether it's unique to ME. I wonder where ATP/ADP depletion would fit in with the description given of ME (ICC) here:
Postexertional neuroimmune exhaustion is part of the body’s global protection response and is associated with dysfunction in the regulatory balance within and between the nervous, immune and endocrine systems, and cellular metabolism and ion transport [42–46]....

Numerous papers document abnormal biological responses to exertion, such as loss of the invigorating effects of exercise [20], decreased pain threshold [47–49], decreased cerebral oxygen and blood volume/flow [50–53], decreased maximum heart rate [54], impaired oxygen delivery to muscles [55], elevated levels of nitric oxide metabolites [56] and worsening of other symptoms [57]. Patients reach the anaerobic threshold and maximal exercise at a much lower oxygen consumption level [58]. Reported prolonged effects of exertion include elevated sensory signalling to the brain [59] that is interpreted as pain and fatigue [29], elevated cytokine activity [60], delay in symptom activation [61] and a recovery period of at least 48 h [57]. When an exercise test was given on two consecutive days, some patients experienced up to a 50% drop in their ability to produce energy on the second evaluation [62]. Both submaximal and self-paced physiologically limited exercise resulted in postexertional malaise [48].
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
The name ME was given because they found CNS inflammation. By definition, without the CNS inflammation, it is not ME.

Without wishing to stray too far off topic, Guido, might you for my benefit point to where this was established please? I assume it was the result of a research paper that attached the name to the symptomology? Are we talking about the time ME was afforded it's categorisation by the WHO, or perhaps earlier, at the point in time it was being talked about in the Lancet i.e. 1969(?) 1956 respectively? Thanks.
 

Ember

Senior Member
Messages
2,115
.
I'd say that PEM is first of all caused by ATP/ADP depletion.... None of this is unique.
This video, posted by heapsreal yesterday, suggests that ATP depletion is far too general an explanation of fatigue to successfully challenge the more specific claim that PEM, as measure by the Pacific Fatigue Lab, is unique to CFS or that PENE may be unique to ME:

 

Bob

Senior Member
Messages
16,455
Location
England (south coast)
The latest edition of Breakthrough magazine has a summary.

ME Research UK - Breakthrough Magazine:
Autumn 2012 issue, page 13, third column, under 'Belgium':
http://www.meresearch.org.uk/information/breakthrough/index.html

Post-exertional symptoms for diagnosis
There is much discussion about particular
criteria for the diagnosis of ME, CFS, PVFS,
CFS/ME or ME/CFS – just listing these
acronyms makes the head spin. But, in the
absence of hard data from real patients,
much of the speculation generates more
heat than light, and produces more angst
than understanding. That’s why the results
of a recent investigation on patients from
the Maes Clinic in Belgium are so valuable.
The investigators raised the question
of whether clinical differences could be
observed between CFS patients with postexertional symptoms and those without such
symptoms. Using statistical models, they found
that a combination of fatigue, a subjective
feeling of infection, and post-exertional
malaise defined groups of patients in which
distinct differences in clinical symptoms (and
inflammatory biomarkers) could be found.
The researchers’ conclusion was that
whilst the traditional (Fukuda) definition of
CFS can adequately distinguish between CFS
and uncomplicated ‘chronic fatigue’, patients
fulfilling the Fukuda definition should be
subdivided into those with post-exertional
malaise and those without. Interestingly, the
UK’s NICE Clinical Guideline of 2007 insists
that post-exertional symptoms should be
present for a diagnosis of ‘CFS/ME’ to be
made, so the importance of post-exercise
symptoms is already recognised formally. The
challenge remains to get GPs and healthcare
professionals to apply the criteria in practice
when diagnosing patients in the clinic.