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by Martin Butler
Part 2
The fundamental error of suggesting CFS is on some fatigue continuum is present. The emphasis should be on how to differentiate fatigue and prolonged fatigue states from the chronic fatigue syndrome.
That CFS is “currently hypothesised to be due to brain dysfunction” is an unreferenced and unsupported assertion. Who and why? There are numerous other hypotheses also. Why are they not mentioned? Is it so that an immediate association to psychological dysfunction can be inferred?
The doctors are encouraged to recognise the reality of their patients suffering and disability. Why are they not encouraged to recognise the reality of the disease? Is it because the authors don’t believe in it? Once again it is inferred that CFS is psychological and therefore not to be treated as a physical problem.
Box 1 is a list of diagnostic criteria. It is not a list of characteristic symptoms.
There are many more symptoms that can be present in CFS. The report contains no extensive list of CFS symptoms.
The separation in Box 1 of fatigue and other symptoms is an artificial construct. It should also be noted by the authors that depression is not a criteria.
We see throughout the report that it is difficult for a doctor to exclude a “psychiatric” diagnosis.
By what medical and scientific reasoning should only a “restricted set of laboratory investigations” be performed on a patient suspected of having CFS. Is the normal approach taken by doctors to diagnose any other disease? No it is not. This recommendation has more to do with setting up a financial model of treatment acceptable to Medicare than to do with proper diagnosis and effective patient outcomes. Laboratory investigations should be selected as the doctor sees fit to properly diagnose the patient and not to stay ‘on side’ with the HIC. Where are your ethics in this recommendation?
You need to decide whether “a protracted recovery period lasting hours or even days” is the case or “recovery is normal (Holmes, Lloyd etc. p.24 box 5.4). From my experience Holmes, Lloyd etc. are dead wrong. Post exertional fatigue and symptom exacerbation are primary recovery problems with CFS.
It should be made clear that many of the clues to “alternative diagnoses” are nevertheless present in many CFS patients as symptoms of CFS and do not necessarily indicate an alternative diagnosis. Doctors grabbing the most significant recognisable symptoms and coming up with that as proof of alternate diagnosis is a common problem for CFS sufferers. Specialists, psychiatrists in particular, are prone to labelling the patient with a condition according to their specialty and ignoring other symptoms. The most significant symptom one day may not be so the next and could therefore indicate a different diagnosis. This is then a lottery of diagnosis for the patient depending on who is the first specialist they see.
The listed disorders for exclusion could not possibly be detected by the recommended screening investigations in the following section. e.g. can a tumour be detected with a scan?
Great care needs to be taken with behavioural signs. Due to CFS brain dysfunction can appear to be evidence for psychological disorder. However these can be transitory depending on the patients current CFS state. e.g. dietary or activity changes can cause significant changes in mood as a result of metabolic changes. This is not recognised by the report authors. They have a tendency (more like a dangerous bias) to get the “horse before the cart” when it comes to psychological impairment due to CFS. i.e. CFS is not due to psychological impairment but psychological impairment is a symptom of CFS.
The omission of the recent Newcastle screening tests is glaringly evident. Oh sure they have not been “validated” but by ignoring them the authors are once again demonstrating their dismissal of physical explanations not to mention possible certainty of diagnosis. But that works against the dogma of psychiatric cause.
Considering that the aetiology of CFS is not discovered, setting a list of tests is totally arbitrary. It is subjective and susceptible to the bias which is already evident elsewhere.
The recommendation against investigating some indications is an evil sentencing of some presenting patients to under diagnosis or non diagnosis of disease. The only support for such arguments is once again to serve Medicare and not the patient.
There is a real need for CFS specialists. It is apparent from the large number of misdiagnosed patients that neither the average GP or the standard specialists, whatever their specialisation, has much of a clue about CFS as an entity. They all grab the bits they know and try a treat them. The ignorance and self interest which continues to be evident in this report is scary for the average CFS sufferer.
Spreading a patient around depending on the worst symptom or sending them to a gaggle of specialists to treat each different symptom is ludicrous in the extreme also. CFS symptoms do not respond in the same way as individual unassociated symptoms in other diseases.
Focusing “on key symptoms that might suggest alternative explanations for the fatigue state” (sic) is the best way to create a misdiagnosis and miss CFS as the primary diagnosis. CFS is acknowledged by the report as an heterogeneous disease that affects multiple body systems. It doesn’t fall into any existing specialists area of expertise so a whole body specialist is called for to diagnose and treat real CFS cases. There are some doctors who look for indicators of CFS rather than excuses to eliminate them. The inference from this recommendation is once again that CFS is not a real disease.
The first sentence is very confusing. Is it referring to prolonged fatigue or to CFS. CFS does not usually “resolve spontaneously”. There is no evidence for such a statement in respect to CFS. In any case to then suggest that reassurance and supportive care is generally all that is required” is, as I have already said, therapeutic nihilism.
To give a prognosis for CFS once it is diagnosed is all very well, but what is the prognosis? It is certainly not “spontaneous” resolution!
Doctors who provide their patients with effective treatment are the ones who develop beneficial therapeutic relationships. Empathy and a non-judgmental style are worthless without it. It should be understood that CFS patients come to realise when they are being patronised. I find the list of items for managing people with CFS rather interesting. I will address them one at a time.
Once again doctors are asked to clearly explain a disease which as yet does not have a clear understanding. But the dogma is the report writers saviour here again also. Any idea that CFS may have physical origins is dismissed as “simplistic attributions”. That only leaves psychiatric origins.
I fail to see why, once a PwCFS has been diagnosed that encompassing ... psychological ... aspects of the individuals disability is more appropriate” unless CFS is a psychiatric illness which is what the dogma of this report wants us to believe.
And here of course CBT comes to the rescue because “no pharmacological agent has reliably been shown to be effective in the treatment of CFS”. But why then are they the preferred intervention for symptomatic relief especially when “people with CFS have increased susceptibility to drug side effects” and whose “response cannot be predicted” (p. 3). Why of course, we are really treating a psychiatric illness aren’t we and they respond well to drugs, especially antidepressants!
This is actually true. Some level of activity is necessary to prevent deconditioning and a lowering of symptomatic exacerbation thresholds. However, don’t forget that it is the improving CFS that allows increased activity and not the increased activity that brings about the improvement. Therefore it should read “if exercise tolerance improves” otherwise it is just CBT claptrap that assumes increased activity is the cure.
Contrary to the inference of the second paragraph, it is very important to note that the disturbed sleep patterns in CFS are a result of the disease and not the disease a result of disturbed sleep patterns. Of course they do not help recovery either.
Avoiding day time naps may be impossible for many CFS patients due to the extreme exhaustion they endure as part of each day.
Many CFS patients have compromised immune system function and the use of analgesics etc. tends to reinforce dysfunctional cycles rather than restore this function. Better approaches are available than the tired old resort to drugs, none of which has “reliably been shown to be effective in the treatment of CFS” and have “harmful side effects” to PwCFS who “may have increased susceptibility to drug side effects”. They “do not induce normal sleep” (p. 21) either.
As it has been hypothesised by some researchers that drugs such as sedative hypnotics actually entrench deranged cycadian rhythms, a better solution to drugs is corrective techniques such as relaxation and mild herbal formulations and treatments that address the underlying CFS.
There is no scientific evidence to suggest drug treatments are any better than other types of treatments that have been comprehensively ignored or ridiculed in this report. In fact there is evidence that drugs are harmful and cause increased side effects.
The agenda is exposed when the authors state “the illness as a whole cannot be attributed simply to major depression”. CFS has not been attributed to major depression at all. In fact it is not known what causes CFS. This statement is entirely unscientific and baseless. However the authors wish us to believe CFS is attributable to major depression.
The “reasonable approach” is nothing more than experimenting and thus has no credible bases. Here is once again an opportunity to plug for the specialist “to guide the choice of drugs”. GPs need not apply.
According to the “exhaustive review” Fibromyalgia was not researched. On what basis then is this assertion included as support for using analgesics, NSAIDS and tricyclic agents. Where is the research to support it? It is, I suggest, included to prop up the dogma of psycho-pharmacological treatment.
The second paragraph leaps straight into “a successful return to work or school” “after a prolonged illness with (sic) CFS”. Where are the recommendations for psychological and social support for during the course of CFS? Once again we are presented with a patronising attitude to mask the real attitude of the authors that CFS is psychological and the patient merely needs a helping hand to pull themselves back together and return to work.
This list of questions and answers are an autocrats dream come true. The answers are once again one sided dogma with any if, buts or maybes omitted or included to support the preferred view as required. Significant questions are omitted such as ‘Are the side effects of drugs unpredictable?’ and ‘Is the unstated assertion that CFS is a psychiatric disorder a baseless one? and ‘What proof is there that CFS is a form of depression and not physical?
This table is unworthy of the profession and most CFS patients will find it offensive as I do.
The 3 sections that follow the overview are an elaborate but transparent construct to establish CFS on a fabricated continuum of fatigue. The continuum could in reality be any of several, such as pain but that doesn’t suit the agenda. They then introduce psychiatric terms such as neurasthenia and facts (irrelevant to CFS) such as “when adults present for medical assessment with fatigue states the most common alternative diagnosis to consider is major depression” (p.9) and “most people with depressive disorders present to primary care complaining of fatigue” (p.10) in an attempt to prove that CFS is a psychiatric condition. They enforce this dogma by asserting that any one sensible enough to reject such a hypothesis has a somataform disorder.
The model is then illustrated with a fanciful diagram that proves this association by showing that CFS and Depression (and anxiety) all have the common component of fatigue. We can of course discount the physical syndromes of Fibromyalgia and IBS because Chapter 6 removes them from consideration.
To add credibility to the argument carefully selected patient and support group “perspectives” are sprinkled around, selected mainly for their psychological inferences or to plug for specialists and drug therapy. None are evident supporting alternate therapies.
We are then told the benefits of this diagnosis (p. 14) are to know what is wrong (even though’ no one knows that yet with any scientific certainty so this is rather fanciful); that we will all get along now if you don’t question the (psychiatric) diagnosis and treatment (drugs and CBT); and by golly if you do you will be punished with longer term morbidity.
And you are really asking for it if you “create or perpetuate myths about aetiology, natural history and treatment rationales which themselves increase disability” by “Inappropriately linking simple biomedical notions of disease (e.g. infection or poisoning [physical]) with complex forms [psychiatric] of ill-health (notably chronic fatigue [not CFS, they don’t state that, just imply it]” or you “may create artificial concepts such as ‘chronic viral infection’ and ‘chronic immune deficiency’” because that may then “actively promote chronic ill health, life time disability” etc. “Such overly simplistic notions tend to minimise the important roles of social and psychological factors in determine the course of chronic ill-health.” (p. 14)
WOW! The drawbacks of not seeing it their way. The Nazis would have loved such eloquent propaganda. So don’t even think about questioning the high priests of the psychological dogma.
Is it worth continuing to comment when such rubbish is being rammed down our throats? CFS patients might be cognitively impaired but we are not stupid.
The authors continue with their collective heads in the sand linking fatigue and CFS as if they are on a continuum. The data presented in the tables on p. 16 are not reliable because the samples are not homogeneous. This would be highly probable in the face of the diagnostic and treatment method recommended in this report that lumps CFS and fatigue illness together on a continuum. The sharp differences in recovery rates (table 3.2) may indicate two distinct conditions and a perhaps a high misdiagnosis rate amongst Wilson and Sharpe’s samples. Their improvement rates are similar to fatigue only samples of table 3.1. Their recovery rates are predictably low because they would have been treating patients for depression related fatigue instead of for CFS which is probably a physical illness and would respond accordingly.
I have not read the paper but Vercoulen’s fluoxetine, no doubt used as a psychiatric agent, could be the culprit for low recovery and improvement rates in his study, not the belief in a physical cause for CFS.
As any physical attribution for CFS has been eliminated, there are only two treatments left available. Drug therapy and CBT and that’s what we get. Apart from the fact that it appears Sharpe’s CBT trial has significant problems concerning subject group it comes recommended without reservation. This wouldn’t all be bad if we could be confident that the CBT that was being offered was focused on assisting recovery from a physical illness and the secondary psychological effects often associated with disability. However the thrust of the report continues according to type and the heavy emphasis on parallel use of anti-depressants for psychiatric management of CFS is supported with a considerable degree of bias.
What is stated as a disqualifying feature of antiviral, immunoregulatory and metabolic drug regimens (“no agent consistently demonstrated efficacy”) is ignored for antidepressants (“empirical evidence from trials is limited”, “limited evidence of benefit was observed” and “showed no more benefit than placebo”) (p. 19) which are wholeheartedly endorsed (p. 3) and recommended using a tenuous link to fibromyalgia as extra evidence for use. Do the authors have a ‘dependency’ on these drugs? Once again fibromyalgia is included in the research when it is convenient to do so in contradiction to section 6.
Items in table 4.3 are dismissed without further qualification. One is to assume they didn’t meet the conveniently ‘revised’ evidence ratings, or is it simply that no one actually looked.
Table 4.2 is another blatant example of self serving. Lloyd and Wilson’s trials both get the “further studies recommended” tag on grounds no better and possibly more favourably reviewed than other poorly reviewed treatments with just as good a level of evidence such as Behan’s EFA etc. regardless of the recommendation that they “warrant further investigation”. (p. 22).
The vortex of figure 4.4 has such a wonderful spiral into Disability that it is a wonder the authors have not seen the irony of their deceit.
No wonder “members of CFS support groups” have an increased “alienation from medical and government agencies” (p. 21) if this report is representative of the “scientific evaluation” that is foisted upon them!
The second section has actually got something good to say about knowledge gaps and heterogeneity but unfortunately falls back on the unproven symptomatic drug therapy as a cornerstone of management.
If only they would open their eyes to the clues screaming at them from tables 5.1-5.4 trumpeting “conflicting evidence” and they might realise there is something fundamentally wrong with their analysis of CFS indicators that confirm findings such as those of McGregor’s groupings of CFS patients by urine metabolites. Martinovic has done useful (unpublished) work on CFS “states” which is why he got such good results. Any statistician worth his salt could come up with meaningful data if CFS patient samples were more specifically evaluated. But alas I fear the dogma requires an amorphous mass of meaningless data from fatigued individuals so that the religion of the psychiatric high priests can own CFS for yet another day.
To end on a positive note, I like figure 5.5 although I remain suspicious of just what the authors mean by “abnormal brain function”.
Martin Butler
March 1998
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Moira A Smith - Canberra, Australia
last revised 8 March, 1998