CONTENTS
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.
Context
“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.
Conclusion
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, Imprint-Academic.com, 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
http://www.investinme.org/InfoCentre%20Guidelines.htm#Canadian_Criteria
