The New International Consensus Criteria for M.E. - content and context


By Bruce M.Carruthers, MD,CM, FRCP(C).

This article was first published for the Journal of IiME Volume 6 Issue 1

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Sir William Osler said “Look wise, say nothing and grunt. Speech was given to conceal thought.”

This is a typically Canadian form of advice. As a compatriot, it is with great trepidation that I deviate from it.

In the new ICC the general thrust of the 2003 Canadian Consensus Criteria is retained but developed further.

§  We recognize the international scope of the problem of ME and its solution by moving to an international consensus panel.

§  The 6 month waiting period is no longer required, but left to clinical judgment.

§  The distinct dynamical symptom pattern of Post-Exertional-Neuroimmune-Exhaustion is kept criterial and further articulated as having the dynamical structure of unusual physical and/or cognitive fatiguability after the appropriate kind of exertion, which may be immediate or delayed, and has a prolonged recovery period.

§  Other symptoms and signs arising from dysfunction within the following subsystems often share a coherent dynamics with PENE, to suggest an interactive underlying causal context- neurological (neuro-cognitive, pain processing, sleep disturbances, neuro-sensory and motor), immune, gastrointestinal, genitourinary and endocrine subsystems, as well as dysfunction in the energy production and transport systems-cardiovascular, micro-vascular, respiratory, and maintenance of thermostatic homeostasis and intolerance of temperature extremes).

§  Interactive dynamical pattern matches between the criterial PENE symptom pattern and the symptom/sign patterns arising from other patho-physiological subsystems are first articulated in individual patients and then as projectable in individuals, if they remain coherent and consistent over time, as well as onto larger groups of similar patients. Thus these observations become mutually confirmable as pointing to real and natural structures/patterns/kinds that  exist “out there” as part of the causal structure of the body in its world- and not as creatures of the mind that happens to be  trying to observe and re-present it (nominalist, constructed kinds).

§  Modulations for paediatric cases are added.

§  Exclusions that are likely to become necessary for the individual case as part of her/his differential diagnosis are listed.

§  The ICC keeps its focus on selecting relatively homogeneous subsets of patients with interactive symptoms, essential for  clinical research if its observations are to be properly controlled, while including a discussion of recent pertinent research results.


“ME” as the name for a chronic fatiguing disease of bio-pathological causation has a long history, primarily  in the U.K., even though the specific bio-hypotheses of causation underlying its name proved difficult to confirm, given the technology available at that time (1954-94).  Over vigorous objections, the name then largely shifted to “CFS”, a noncommittal umbrella disease concept that includes all fatigues that are  severe, chronic and unexplained, but ignores the “syndromeness” embedded in its etymology by putting  symptoms onto lists that ignore their dynamical relations of causal inter-activity. This latter points to a common underlying causal structure, however complex and currently unknown, and  is found in the etymology of the word  “syndrome” (Gk. running together). However elaborately symptoms are entered  into lists, the problems resulting from this neglect of their natural inter-active dynamical  causal structure will remain.

  • In his study of the Reeves criteria for Chronic Fatigue Syndrome, Jason et al found that only 10% of patients identified as having CFS actually had ME, and confirmed the efficacy of the Canadian criteria in separating out this 10% subset.(J Disabil Pol Studies 2009; 20: 91-100).

  • Why was this maneuver of the Canadian criteria so effective in separating out this subgroup? By recognizing  that fatigue showing the  specific dynamical patterns of ME  characterized  a large subset of fatigued patients, and thus was different in kind from the patterns underlying  the majority of severe, chronic and unexplained fatigues (CFS).  It thus pointed to a different underlying causality- a natural kind or real pattern whose underlying causal organization lies in the world, not just our representative models of the world, that could be researched using biological methods- given adequate comparative controls.

  • With major advances in technology, recent research guided by properly scientific hypotheses has given strong support to “ME”s implication that  a different underlying causal structure- one involving inflammation and dysfunction within the CNS, ANS and immune systems, plus more- underlies this large subset of CFS patients.

  • While it has always been essential, it has now also become urgent to segregate the subset that we are calling ME more clearly, using the ME  International Consensus Criteria, so that researchers can  confirm/disconfirm their results using  patients who have chronic fatigue of this clearly bio-pathological origin. Otherwise the all-inclusive umbrella of “CFS”, in ambiguating natural and psychosocial kinds of fatigue, will continue to dilute the results of any investigations and maintain the pervasive confusion resulting when biopathological kinds are mixed indiscriminately.


  • The results of Jason et al’s studies have confirmed that the Canadian Definition of ME/CFS had clearly separated cases who have ME (fatigue of bio-pathological or natural origin, arising out of  a pathological causal structure present in  the world apart from the mind that is observing it) from those  who have CFS (which includes the   minority of the specific natural kinds we are calling ME plus a majority of fatigue kinds that are secondary to other diseases, plus parts of  the normal homeostatic activity-rest cycle designed by evolution, plus fatigue kinds constructed by the re-presentational observing/thinking and thus dualistic model-making mind).

  • The prevalent use of symptom-based definitions has been adding to the confusion by analyzing complex syndromes using a Cartesian method of  analysis that isolates symptoms by putting them onto standardized lists of separated subjective entities, thereby bypassing the dynamical subjective/objective interactive processual causal on-line context that points to an underlying interactive causal organization, even if we are as yet unaware of its details.

  • Contrariwise the new ICC encourages that symptom structure be observed on-line as interacting  embodied and embedded causally interactive  dynamical process(es) that have multiple subjective/objective manifestations. These  are first observed (or ignored) in a clinical dialogue as (subjective) symptoms and (objective) confirmatory signs which are disambiguated on-line, in their natural context, as temporally dense and as having  felt/observed causal efficacy. These individuated observations are in turn confirmed by objective biochemical measures, pathophysiological functional testing and imaging. The “same” phenomena can also be studied off-line using epidemiological studies which observe the generalisable constancies found in groups of variously homogenous  groups of cases using standardizing techniques of questioning and observation to obtain generalisable results and case definitions. In the standardized and properly randomi­zed environments  of scientific experiments, the effects of interventions can be properly controlled, and thus general rules of causality inferred and quantified.

  • As the ICC panel members add clinical guidelines and symptom scales (ICSS), these three essential kinds of observation will be integrated by using a transductive and mutually confirmative language that matches the dynamical causal patterns to be found in each realm.  This pattern “language” must be flexible enough to negotiate the changes in scale and context involved in comparing observations arising from disparate clinical, epidemiological and research methodologies, scales and contexts, all of which necessarily remaining distinct, yet interrelated. We are confident that this will lead to mutually confirmed outcomes that can be generalized and standardized world-wide- meanwhile remaining adequate to the particularities and demands of each patient’s complex illness/disease structure.

  • As Osler also said “Listen to your patients. They are giving you the diagnosis”. Now we have the technology to confirm this directly for this complex disease- if we use it.

 Since this presentation was given in Ottawa Sept 24, 2011, the Journal of Internal Medicine has published 3 articles concerning these issues that are freely accessible on line-

1/ The ICC for ME was published- J Internal Med Oct 2011, 270: 327-38.  

2/ A critique-   ´A controversial consensus” published  JWM van der Meer and AR Lloyd J Internal  Medicine 271: 29-31, Jan 2012. In particular the above authors discussed the “unscientific” way the ICC was laid out, discussing the  “pseudoscience of pathophysiology” “notional” pathophysiology,  and the “intrinsic heterogeneity in syndromal diagnoses” but neglecting to mention how their  recommended approaches to syndrome description had contributed to this situation by treating  symptoms as separated subjective things on lists, thereby destroying any consideration of their embodied interactive  dynamic context or “syndromalness”  (Gk etymology, running together on a track), and rendering research directed towards underlying causality more elusive.

3/ A rebuttal of the critique by G Broderick J Internal  Med vol 213-17 Feb 2012. corrects some of these misapprehensions, and points out that the Reeves and Oxford criteria for CFS select patient sets that are approximately 10x larger and more inclusive than those selected by the Fukuda criteria, and that the Canadian consensus criteria selected patients with even more severe physical functional impairment, less psychiatric comorbidity  than the Fukuda definition(see Jason et al Am J Biochemistry and Biotechnology 6: 120-135, 2010) and obviously brought to salience the distinctive pathophysiological pattern of delayed reactive fatigue, which it made criterial.  

This symptom is not the simple name of an isolated  subjective feeling put on a list, but points to its participation in a higher level fatigue/activity control network which we know to be present by its disregulated causal efficacy in the world, even if we do not yet know what its details are, and which we are calling “ME” in honor of the earlier  (and current) sufferers and prescient observers of this kind of suffering. Other earlier and revised case definitions based on the disease concepts of Ramsay had made postexertional malaise and impairment of memory and concentration central to the diagnosis of ME (Lloyd AR et al Med J Aus., 153: 522-528, Goutsmit, E et al Health Psycholog. Update 18:27-31), but  none before the Canadian Definition of 2003 had made this specific dynamic and projectable pattern of pathological fatigue criterial for the diagnosis of ME/CFS, and the ICC case definition of ME is carrying on and developing this strategy further. The specificity of this illness pattern provides a level of detail that is necessary for patients to adapt to the aberrant pattern of fatigue as experienced in their own illness using pacing. Research can be designed to study the pathogenetic details of this particular pattern and the many others that I expect will be uncovered as the ICC strategy is used more widely, with the assurance that results are not being continually diluted out by the 90% majority of CFSers who don’t have this kind of fatigue pattern. We can finally search for specifically directed remedies. This is the way towards scientific progress after what has been a long delay, indeed a paradigm war- not arguments between results but between opposing assumptions made before beginning observations.

 All three of these contributions agree on one point- that whatever it is we are talking about, it is a complex disease/illness- but on little if nothing else. There was special confusion on whether we were talking about CFS or ME, regarding them as mutually exclusive dualistic entities and not complementary parts of a single disease concept. And confusion reigns about what we mean by complexity itself in various realms (the topic itself is complex)- and we are dealing with the realm of medicine, where not much serious thought has been put to it as yet, e.g. producing long symptom lists and symptom counts doesn’t help.

 Simple or Complicated structures have a known stable causal structure, of variable intricacy, that hence are predictable if you can extrapolate from knowledge garnered from one astute observation.  Complex structures do not, as their causal structure is forever recursively changing-as a result of the causal interaction of their constituents-and hence are inherently unpredictable.

As a consequence a complex structure must be observed continually, while the complicated one does not have to be, while confirming/disconfirming inferences, tests, and imagings are made. For complex diseases the only observer who is constantly observing the patient is the patient her/himself. We all must learn to utilize this kind of continual common sense self-observation by patients in dialogue with their physicians, as we together observe the development of complex diseases over real time through a robust and productive doctor/patient relationship. This will entail a large qualitative shift in attitude and appreciation of the value of the direct self-observation of illness structure as it evolves in real time, if done properly- and without diversion into cognitive dualisms.

 There are also repercussions of post-cognitive  theoretical moves in psychology into direct non-representational  perception and radical embodied cognitive science ( see  “Radical Embedded Cognitive Science) Anthony Chemero MIT Press, 2009 and  “The Mind, the Body and the World- Psychology after Cognitivism? Ed. B Wallace, A Ross, J Davies and T Anderson,, 2007.), which point to the need for a distinct shift in strategy (in our realm of medicine)  from its current emphasis on developing generalized cognitive disease models to directly observed, individuated  diagnosis of illness and its therapeutics. This is also emphasized by the development of bottom-up systems biology and translational and systems medicine (Nielsen J.J Internal Medicine 271, pp 108-110). Our current treatment of symptoms and syndromes in diagnosis and prognosis, and of pacing and the role of self-organization in therapeutics, will also need great adjustments as we move from an “anthropogenic” to a “biogenic” approach to them. (see “The biogenic approach to cognition”  Pamela Lyon, Cognitive Processing 2007: 11-29) .

 Opportunities are arising with the rapid development of technology to allow direct confirmation of the clinical symptoms and signs observed by  individual patient/physicians without a detour through the medical model, but by attending to directly observed individual illness structure, with mutual transductive confirmation of the symptom patterns felt directly by a patient in dynamically congruent patterns observed within the  under-overlying causal systems at different OMIC scales (genomic, cellular, organ, physiological system, as well as at the  emergent organismic, organismic/environmental/ epidemiological, etc. scales.

  What is in process for our ICC endeavour are the preparation of  an ME Physicians’ Primer/Guidelines and the preparation and testing of an International Symptom Scale to improve cross-standardization of  symptom questioning when comparing groups of patients where  clinical epidemiological  and other statistical  studies are being planned.

Further Reading

Guidelines - and Canadian Guidelines

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