state how many of those citations were made by himself as a prolific
author or by his colleagues.
He also mentions that he developed the prototype that became known as
the Chalder Scale - which has been shown to have a ceiling meaning it
measures normal but not does not distinguish pathological fatigue.
Jason et al 2011 states, "As an example of a measure of fatigue
intensity alone, Chalder et al.'s (1993) Fatigue Scale is a 14-item
verbal rating measure that has strong internal consistency. Using an
ROC curve analysis, Jason et al. (1997) found this scale was able to
discriminate a CFS sample from a healthy control sample; however, it
was not possible to differentiate the CFS sample from a lupus or
multiple sclerosis (MS) sample."
http://dsq-sds.org/article/view/1375/1540
J Neurol Neurosurg Psychiatry. 2012 Jan;83(1):4-5.
Impact Commentaries. The nature of fatigue: a comparison of chronic
"postviral" fatigue with neuromuscular and affective disorders.
Wessely SC.
Department of Psychological Medicine, Institute of Psychiatry, King's
College London, London, UK. simon.wessely@kcl.ac.uk
Accepted 17 August 2011
The nature of fatigue: a comparison of chronic =E2=80=9CPostviral=E2=80=9D =
fatigue
with neuromuscular and affective disorders1
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 =E2=80=98proper=
=E2=80=99
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=E2=80=94they 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=E2=80=94=E2=80=9CDear Simon, Please se=
e this
patient. There is nothing wrong with her=E2=80=9D.
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 =E2=80=98ME=E2=80=99, short for myalgic encephalomyelitis, which f=
urther
irritated the neurologists. In the media it was known as =E2=80=98yuppie fl=
u=E2=80=99.
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 =E2=80=98hit=E2=80=99. And basi=
cally 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 =E2=80=98chronic postviral fatigue=E2=80=99 pat=
ients (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=E2=80=94600 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=E2=80=94that 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=E2=80=94as 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 =E2=80=98ME=E2=80=99.3 That would prove t=
o 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 =E2=80=98yuppie flu=E2=80=99, and that it also was not untreatab=
le.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 =E2=80=98all in the mind=E2=
=80=99 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.
=E2=80=9CIt is not our intention to adjudicate between the opposing views o=
f
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=E2=80=9D.
Any lessons? You can do important research with minimal resources. We
never had a grant for it=E2=80=94the 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.
Footnotes
Competing interests None.
Provenance and peer review Commissioned; not externally peer reviewed.
References
=E2=86=B5 Wessely S, Powell R. Fatigue syndromes: a comparison of chronic
=E2=80=9Cpostviral=E2=80=9D fatigue with neuromuscular and affective disord=
ers. J
Neurol Neurosurg Psychiatry 1989;52:940=E2=80=938. [Abstract/FREE Full text=
]
=E2=86=B5 Cleare A, Bearn J, Allain T, et al. Contrasting neuroendocrine
responses in depression and chronic fatigue syndrome. J Affect Disord
1995;35:283=E2=80=939.
=E2=86=B5 Halpin D, Wessely S. The VP-1 antigen in chronic postviral fatigu=
e
syndrome: a controlled study. Lancet 1989;i:1028=E2=80=939. [Medline]
=E2=86=B5 Bonner D, Butler S, Chalder T, et al. A follow up study of chroni=
c
fatigue syndrome. J Neurol Neurosurg Psychiatry 1994;57:617=E2=80=9321.
[Abstract/FREE Full text]
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