Simon Wessely revisits some of his early work on chronic fatigue syndrome, journal article, March 2012

March 23, 2012

J Neurol Neurosurg Psychiatry 2012;83:4-5 doi:10.1136/jnnp-2011-301216

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Simon C Wessely
Correspondence to Professor S Wessely, Department of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK
Accepted 17 August 2011

The nature of fatigue: a comparison of chronic “Postviral” fatigue with neuromuscular and affective disorders(1)

Authors: S Wessely, R Powell

Year published: 1989

Number of times cited: 344

Simon C Wessely from King's College London describes starting out in the early years of chronic fatigue syndrome with his first ‘proper’ paper

In 1987 I was a senior registrar on the Maudsley psychiatry training scheme when I was moved at short notice up to the National Hospital for Neurology, London, because the current SpR, Ray Dolan, had just been promoted to consultant. I soon expressed an interest in seeing one group of patients who were always getting referred to the liaison service, and frankly were not popular with many of the neurologists who ran the place. It wasn't the fault of the patients—they had symptoms that might have had a neurological explanation. But when the neurologists drew a blank, the patients soon got the message, whether rightly or wrongly, that the neurologists thought that they were at best suffering from depression, at worst making it all up, either of which appeared to be confirmed when the next port of call was myself. I still treasure the briefest but still most unintentionally revealing referral letter I have ever received—“Dear Simon, Please see this patient. There is nothing wrong with her”.

That something was wrong was clear, but what exactly? The Americans would introduce the term chronic fatigue syndrome (CFS) a year later, which at least gave a label that doctors could use, but in 1987 it was known as ‘ME’, short for myalgic encephalomyelitis, which further irritated the neurologists. In the media it was known as ‘yuppie flu’. Some suggested it was a postviral condition, others a persistent virus similar to HIV, but the commonest from either patients or the media was that something was wrong with the muscles.

I was however struck not by the overlaps with muscle disorders but with some of the symptoms that I had seen in depressed patients before I came to Queen Square. It dawned on me that I had a wonderful opportunity to test this out, since one thing that the Square was not short of was people with well characterised neuromuscular disorders. So I decided to carry out a simple clinical study, comparing the pattern of fatigue and fatigability in the CFS patients compared with those with illnesses such as myasthenia gravis. I enlisted the help of Robin Powell, another psychiatric trainee, to recruit a second control series of patients with major depression who were being treated at the Royal Free Hospital London.

There was no instrument available to measure subjective fatigue, so I simply invented one, which would later get modified into the Chalder Fatigue Scale, which also became a citation ‘hit’. And basically that was that.

What we showed was clear. The pattern of fatigue in the CFS patients was different to that seen in those with peripheral neuromuscular diseases, and instead was similar to those in the affective controls. The only time when the neuromuscular patients did look like the ME patients was when the former group also had comorbid depression. But there were also differences between the ME patients and the depressed control group that Robin had recruited, although these differences were not as great as those between the CFS patients and those with myasthenia. The CFS patients did not show core cognitive features of depression, such as guilt or self blame. We wondered if this was a reflection of their different pattern of attribution (blaming an external cause, namely a virus, rather than an internal cause, as the depressed patients did). Overall, however, our principal conclusion was that the fatigue in the ‘chronic postviral fatigue’ patients (as we labelled them, knowing that ME would be unacceptable to the journal) had a central, not peripheral, origin, and that primary muscle disease was therefore an unlikely explanation for the symptoms and disability that the patients showed.

The paper was accepted without revision—600 papers later that still hasn't happened again. I wasn't aware of citation indices back then, and it was many years before I was aware that it was indeed a citation success. I think the reasons were twofold. Firstly, it was indeed a piece of pure clinical research, and one did not need either a background in advanced neurosciences or advanced statistics to understand it. Secondly, it made sense, by which I mean that it fitted with what many clinicians already felt—that this was a genuine condition, which bore more relationship to disorders such as depression than neuropathy or myopathy. True, papers were published showing abnormalities in the muscle, but these were most likely secondary rather than primary findings.

Has the paper stood the test of time? Not badly, all told. I think we probably overestimated the links with affective disorder (and when I went back to the Maudsley we then did a neuroendocrine paper which was the first to suggest that there were some biological differences between major depression and CFS2) and underestimated the influence of anxiety. Over the years antidepressants have not proven that helpful in managing CFS, unlike the CBT model that we developed the following year. No compelling viral or immunological biomarker has been found. This is not as some claim for want of trying—as we were doing the interviews for the JNNP paper we also collected samples for a blinded study of the VP 1 antigen, which had been claimed to be a specific enteroviral marker and a test for ‘ME’.3 That would prove to be one of many false dawns in the story of CFS. It still seems to me that the most fruitful avenue for research is going to be via neurosciences, and understanding the nature of the sense of physical and mental effort, which is at the heart of the condition.

How have I stood the test of time? I had really enjoyed doing the research that led to the JNNP paper, and for the first time started to seriously think about a career in academic as opposed to clinical psychiatry. With help from Maria Ron, I put together a successful application for a Wellcome Training Fellowship in Epidemiology, and went to the London School of Hygiene to do the MSc and subsequent doctorate in epidemiology. I continued for the next decade to work on problems like CFS, and had some successes. We showed for example that it was not ‘yuppie flu’, and that it also was not untreatable.4 It wasn't plain sailing though, since it was impossible to get rid of the stigma of being a psychiatrist, which transferred itself to the patients. I found, and still find, that hard to accept, but it was a fact of life, and I became identified with the ‘all in the mind’ view of CFS, which was ironic since my interest in the condition was triggered by the fact that I did not think this was an imaginary or non-existent disorder, as many did at the time. Eventually I would move on academically, even though I continue to see CFS patients clinically.

I may have moved on but some things have not really changed. Re-reading the 1989 paper, I am struck by what we wrote in the discussion. In the intervening almost quarter of a century our observation on clinical bias has been partly addressed, but the rest remains as true as ever.

“It is not our intention to adjudicate between the opposing views of physical or psychological aetiology. With the expanding knowledge concerning the biological basis of many psychiatric illnesses such a division becomes increasingly meaningless. However, both patients, and some doctors, continue to insist on such distinctions. It is instead our purpose to point out the serious consequences that result from this division. Not only will this lead to bias in research based on general hospital samples (as most has been), but it also suggests that many patients are being deprived of effective treatment”.

Any lessons? You can do important research with minimal resources. We never had a grant for it—the only costs were those of photocopying the questionnaires, which I used to do on the ward in the evening when the rather fierce ward clerk had gone home. I am still waiting for the bill.


Wessely S, Powell R: Fatigue syndromes: a comparison of chronic “postviral” fatigue with neuromuscular and affective disorders. J Neurol Neurosurg Psychiatry 1989;52:940–8.

Cleare A, Bearn J, Allain T, et al: Contrasting neuroendocrine responses in depression and chronic fatigue syndrome. J Affect Disord 1995;35:283–9.

Halpin D, Wessely S: The VP-1 antigen in chronic postviral fatigue syndrome: a controlled study. Lancet 1989;i:1028–9.

Bonner D, Butler S, Chalder T, et al: A follow up up study of chronic fatigue syndrome. J Neurol Neurosurg Psychiatry 1994;57:617–21.

8 thoughts on “Simon Wessely revisits some of his early work on chronic fatigue syndrome, journal article, March 2012”

  1. ‘The Americans would introduce the term chronic fatigue syndrome (CFS) a year later, which at least gave a label that doctors could use, but in 1987 it was known as ‘ME’, short for myalgic encephalomyelitis, which further irritated the neurologists.’

    Interestingly, it didn’t irritate my neurologist – Professor Behan – who himself diagnosed me with ME in Glasgow in 1983/84 – 4 years before Simon’s ‘involvement’ – I had not heard of ME, at that point, and was just extremely relieved to get a diagnosis, post-Coxsackie virus (which I had not heard of either).

    Maybe Simon was not interested in what was going on north of the border.

    And maybe he had not heard of Dr Melvin Ramsay.


  2. The ‘work’ of Wessely under the ‘Chronic fatigue’ banner and obviously flawed psychological reasoning in terms of explaining M.E, has done nothing but harm to sufferers who’s lives are destroyed and made a misery due to the intensive neurological/nervous system/internal organ and physiological effects of this condition; a patho-physiological-neurological reality supported by the recent work of Dr Perrin.

    Furthermore, given the case/death of Sophia Mirza, it is intelligently observable that M.E is not Chronic Fatigue or of simplistic ‘psychological origin’ at all.

    The truth is, the exact pyhsiological mechanisms causing M.E largely lie outside the fundamentally flawed ‘conventional medical’ paradigm rooted in Newton’s outdated perspective of what constitutes ‘science’. These ‘medical proffesionals’ never seem to question this reality however when M.E doesn’t ‘fit’ into their limited criterias.

    So, instead, they dismiss patients as ‘imaging the whole thing’ or create generalised/overly simplistic terms such as ‘Chronic Fatigue’ to explain phenomena such as M.E that clearly highlights the flaws in their ‘knowledge’ and ‘practices’. Or, in Wessely’s case, furthers his own career and prestige based on obviously flawed ‘papers’ with scant disregard for the dangers inherent in the wider implications of removing the nuerological component in the classification of M.E which has lead to the deaths of sufferers.

    And this, we apparently call ‘health care’; no, this is the consequence of business/dollars/ego now driving ‘conventional medicine’, which in the case of M.E has shown that a remarkable amount of intolerance and intellectual arronagance, is indeed very dangerous.

    How many more people who devlope M.E needlessly have to die or be subject to torture for years on end in isolation whilst the ‘conventional medical establishment’ hides behind philosophical jargon Wessely claims as ‘help’.

    The insanity of the situation regarding M.E given what has unfolded since 1990 and beyond, after the changes in criterior to the ‘Chronic Fatigue’, banner as a result of Wessely’s work, is beyond all reasonable intelligence.

  3. Simon says

    With the expanding knowledge concerning the biological basis of many psychiatric illnesses such a division becomes increasingly meaningless. yes i agree Simon the psychiatric aproach becomes meaningless and a more scientific aproach more apropriate when a biological cause is found ,keep going and you might talk yourself out of a job.
    Spending a few pence on paperclips and some paper on ME that really shows you care?
    Maybe you could sell some string next time and save some bottle tops for your ME patients you also forgot to mention the millions spent or wasted on your psychiatric reaserch. Dont worry Simon i dont mind being deprived of your defective treatment”.

  4. “It still seems to me that the most fruitful avenue for research is going to be via neurosciences, and understanding the nature of the sense of physical and mental effort, which is at the heart of the condition.”

    Have to agree with this bit staggeringly – as long as the research is investigated from a neurological (EEG for eg)/endocrine perspective ie what exactly happens in the brain & body before/during/after the body decides to initiate an action (& not ‘why are patients ‘afraid’ of exercise?)!

    The neurologists have let us down v badly for the most part. They appear to have dismissed M.E. because it doesn’t fit into already known neurological parameters, instead of showing scientific curiosity.

    What if its polio (or Cocksackie B) affecting primarily the sensory nervous system/brain feedback for eg (rather than mainly motor function)?

    What on earth do they think is going on when 250,000 + patients up and down the UK, most of whom don’t know or have never heard of each other, are complaining of almost identical symptoms at the same time? *??@!!!

  5. Hey Jackie, Agree that the stance of some neurologists is bizarre indeed, but how much have they been influenced by the all powerful biopsychosocial lobby over the last two decades?

    Simon is very much back-pedalling, presenting a rather benign view of himself as ‘good cop’ in the entire ME saga, when the opposite is actually true. Each article he now writes, since last year’s carnival of damning PWME in media, is further diluting his role as ‘bad cop’. One has to wonder what he is up to. Is this a slowburning acknowledgement that he was wrong all along?

    And I am surprised that while he is in in such reflective mood that he has not mentioned PACE/GET, a study which he has in the past described as ‘elegant’. Interesting that he is sidestepping that whole abominable episode, which was an insult to every single person who suffers from neuroimmune ME.

  6. I got ME in 1972 (at the age of 12). It was 6 whole years later before I had mental health problems which have remained with me ever since. And are a direct consequence of inadequate diagnosis.
    1 I think therefore I am, this is fine.
    2 I feel it therefore it is, no say the doctors, you feel it but it is a construct of your own brain.
    thus step 3 my senses give me information about the world, can never be achieved because if my own body feelings are constructs how much more so are perceptions of the world.

    Thus down the line my psychiatrist says ‘you suffer from existential angst.’ Well who wouldn’t had they been taught not to trust their own body?

  7. Perhaps you are right about the back-pedalling,nmj. You also make an interesting scathe about SW and Melvin Ramsay. I remember (I think -not noted for my accurate recall!) when SW applied to become consultant psychiatrist to MEA in the later 1980s. Melvin Ramsay threatened to leave his beloved Association if such happened. We all went to London and revolted!

  8. Letter from Countess Mar to Professor Simon Wessely

    Lady Mar has already sent the attached 4 page letter to Simon Wessely

    4th December 2012

    Dear Professor Wessely

    I note from recent correspondence arising from the report in the Independent on Sunday on 25 November 2012, that you believe me as guilty of harassing you. Perhaps it is not surprising that I regard this belief with something less than amusement.

    I wonder whether you recall the time when you were just getting your initial research into Gulf War Illnesses off the ground in mid-1998? I had given evidence to the Royal College of Physicians and Royal College of Psychiatrists Inquiry on Low Level Exposure to Organophosphate Sheep Dip which was published in November 1998. Your colleague, Professor Anthony David, was a member of the inquiry. I recall receiving a letter from you both to the effect that you were sorry that I had had reason to criticise your Gulf War research in the course of my evidence when, in fact I had not mentioned Gulf War research. You also asked to meet me. I recall correcting you on the facts and stated that I had no desire to meet you. I then received a number of telephone calls and letters, both to my office and my home, demanding that I meet you. I have to say that I regarded this as harassment at the time, though I did not see the need to contact the police. Eventually I agreed to accept your invitation to lunch at Gordon’s Wine Bar behind Charing Cross Station.

    I brought with me Ms Emily Green, an eminent scientific journalist, with your agreement. I shall never forget being astounded to find that, when we arrived at the appointed time, 12.30 pm, you had arrived early; bought your own lunch, and presented us with a bottle of water. Prior to the meeting you were very firm about the time, as you had patients to see at 2.00 pm. We discussed a number of topics, including whether you knew Elaine Showalter and whether you had ever advised the Department of Social Security on subjects such as ME. Some of your responses we found were economical with the truth to put it mildly. It was very shortly before 3.00 pm that you finally got to the point – you wanted me to help persuade the Gulf War Veterans to complete your questionnaire!

    I think you need to understand that this encounter left a rather enduring and nasty taste in my mouth, not least because I had to buy my own lunch when you had invited me to lunch. Neither was I impressed by your deviousness in response to straightforward questions. This caused me to look more deeply into what you were doing and into your associations, most of which are now public knowledge. This, in part, helps to explain why I have reason to criticise some of your work.

    I have also attended some of your lectures and have read reports of others. I have heard and read the extraordinary way in which you and some of your colleagues have denigrated people with ME and have tried (and to some extent succeeded) to persuade others that people with ME are not really ill at all; they merely have ‘aberrant illness beliefs’. You have deliberately obfuscated the terminology surrounding ME by linking it with chronic fatigue and attempting surreptitiously to reclassify it as a psychological condition under the WHO ICD classifications. In doing this you appear to have totally ignored the first exhortation to doctors – “First do no harm”. Yet when this beleaguered population has reason to look at your work critically you deny what you have said and written and plead persecution and harassment from the very people you purport to be helping. I would have thought that any thinking person would ask themselves why this is happening; would ask the individuals who are clearly angry what is angering them, and try to put things right. You are in an exalted position – a Professor of Psychiatry with all sorts of awards. Why on earth do you need to play the victim?

    My personal experience with organophosphate poisoning taught me that there are members of the medical profession who are not prepared to “listen to the patient for they will probably tell you the diagnosis”. I am fortunate in that I am articulate and determined and I have been put into a position where I can speak for others less fortunate than I am. If that means offering honest criticism of individuals who, I believe, are hurting others who are not in a position to speak for themselves I am prepared to take any brickbats that come my way.

    So much of the friction comes from people not knowing what you think because you are so inconsistent. For example, in your presentation to the full Board Meeting of the DLAAB on 2 November 1993 which was considering those with ME/CFS you said: “Benefits can often make people worse”, yet in your letter to Dr Mansell Aylward at the DSS you wrote: “CFS sufferers should be entitled to the full range of benefits”. Given that, in 1990 you had written: “A number of patients diagnosed as having myalgic encephalomyelitis ……… were examined …… many of them, the usual findings of simulated muscle weakness were present” (Recent advances in Clinical Neurology, 1990, pp 85 – 131), I am wondering how a genuine condition can also be simulated and am curious to know what your position is regarding benefits for people with ME.

    I note that you do not hesitate to condemn statements from your critics as “the same old stuff that they have been saying about me for years”. People with ME could be equally justified in their belief that you perpetuate the beliefs that you have long held that ME is a psychosocial behavioural problem and that you have totally failed to embrace the vast body of peer reviewed scientific literature that demonstrates damage to neurological, cardiac, endocrine and other systems in people with ME. I believe it was you who recommended that GPs should not indulge patients with too many investigations. This has meant that people with conditions that could have been treated have been misdiagnosed and neglected.

    I have spoken strongly in defence of people with ME who have been traduced by you and your colleagues who have embraced the psychosocial behavioural model. I am not ashamed of having done so for they have few who will defend them publicly. The scientific evidence is heavily weighted against ME being ‘all in the mind’ so, by deduction it must be the economic argument that prevails, to the disadvantage of the estimated 250,000 people who have ME. have you ever considered the savings to the exchequer and to the insurance industry if people with ME were properly investigated and treated so that they could return to work or education?

    I take no pleasure in asking “bogus” questions and making speeches in the Lords. I would very much sooner your profession got its act together and spent some time studying the real effects of ME on patients and looking for solutions. We all recognise that chronic illness, whatever it may be, presents with psychological aspects. CBT can only be a management tool and GET reportedly does more harm than good for patients with ME/CFS as opposed to chronic fatigue.

    Patients must be able to trust doctors and scientists. You have betrayed this trust. A scientist should be able to accept honest criticism. You have misconstrued criticism and turned it into harassment. You have much to answer for, so it ill behoves you to employ diversionary tactics in an attempt to portray yourself as the injured party.

    I have written this as an open letter because so much of this debate has been in the open. It would be helpful if you would make your position with regard to people with ME/CFS utterly clear. Do you still believe the ME/CFS is “perpetuated by dysfunctional beliefs and coping behaviours” as you wrote in your 2002 CBT Manual for Therapists? If you do, please will you explain why no one got better with your model. If you do not, would it not be sensible for you to withdraw it instead of continuing to make the facts fit your theories as they appear to have been in the PACE statistics where you were in charge of the Clinical Trial Unit.

    I look forward to hearing from you.

    Yours sincerely

    Countess of Mar

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