Thursday, March 29, 2007

Tis Spring

Tis Spring, and my allergies and sinuses are combining for a double-whammy.  Nine out of the last ten days, I have woken up with a headache.  Which means that nine out of the last ten days, I would have called into a job sick, because I never know early in the morning whether this is the one that will clear up a little or not.

There have been days where, by late afternoon, I feel up to doing a little work.  But in a "real job" with 8:30 to 5 office hours, by the time I'd decide I could do a little work, and get over there on the bus, it would be the end of the business day.

Yet, despite having this explained to him time and again, the Disability judge stubbornly persists in believing that someone would be willing to offer me permanent employment, no matter how many sick days I take in winter and spring. 

Or that my symptoms would all go away if I got a job.  Except that when I started my own business, my symptoms did not go away just because I had work to occupy my mind -- I did exactly what was recommended to me: focused my thoughts on my work instead of my health, and lost clients every winter and spring because getting out of bed and sitting at a desk and trying to work just made the symptoms worse.  As the symptoms got worse, it got harder to concentrate on the work in front of me.  The pain would reach a point that I couldn't even SEE the work in front of me. 

But my testimony that I have tried to work and had major problems with it was never considered as valid as the judge's speculation that there's an employer with unlimited sick leave who would tolerate all my symptoms and, essentially, pay me for showing up without requiring any actual work. 

If you know such an employer, give them my resume'.  I'll show up when I can, leave when I need to, and do a little work now and then.  On their part, they have to guarantee not to fire me for excessive absenteeism, sleeping at my desk, or the quality/quantity of my work. 

It's nearly noon, and I still don't have it in me to work.  When I tried to proofread this blog post, my headache got worse.  I can type with my eyes closed, but I can't proofread that way.

And so, although I was hoping to get some work done today, I'm going back to bed until the headache lets up enough to do something without making it worse.

Monday, March 26, 2007

Doctor Speaks Out -- Breaks Taboo

I have been taken to task by members of the medical community for daring to expose the truth that some doctors are incompetent and make misdiagnoses.

It will be interesting to see what those same people have to say about "How Doctors Think", the new book by Dr. Jerome Groopman, a Harvard Medical School professor and a honcho at the respected Beth Israel Deaconess Medical Center. After seeing incompetence and misdiagnosis affected friends and family, Dr. Groopman set out to find out how this happens.

Non-fiction author Ron Chernow praises "In this splendid and courageous book, Dr. Jerome Groopman lifts the veil on possibly the most taboo topic in medicine: the pervasive nature of misdiagnosis."

I am very curious to see whether the medical community calls Dr. Groopman the same names they have called me for breaching this taboo, or whether they praise him for finally educating them on how to avoid being sued for malpractice. Quite often, the problem is simply that the doctors didn’t listen. Groopman documents that patients are interrupted, on average, after just 18 seconds. This can be the difference between hearing the two symptoms that are compatible with depression and the third one that changes the diagnosis to CFS. My own medical records prove that doctors don’t listen – there are many things in there that I never said, twisting of facts, and flat-out lies.

For years, I suffered from daily digestive problems. Since the first doctor had convinced himself that I gained weight because I sat in front of the fridge stuffing my face at 3 AM whenever I couldn’t sleep, he missed the real cause. A doctor who did listen, who asked the right questions instead of deciding he didn’t need to ask questions because he knew what the answers would be, solved the problem in minutes, with a bottle of antacid pills that cost a whopping $3.

By listening instead of filling in the blanks with assumptions, he figured out that the problem was not that I was eating at 3 AM, but that I was NOT eating at 3 AM. I’d collapse into bed, exhausted, at 5 PM, too exhausted to get back up, and not eat anything for 12+ hours, leaving my stomach acid nothing to work on. There were times I was too exhausted to fix dinner, and didn’t eat for 18 hours between lunch and breakfast the next day. The only difference between the two doctors was that one "knew" that "every depressed woman eats non-stop" and the other treated me as an individual, not a statistic, asking what I did, not assuming that I do what other women do. (In fact, weight gain from altered metabolism is a common problem in CFS, and has nothing to do with increased caloric intake.)

The very first story Groopman tells in the introduction is very similar to mine: a woman with chronic digestive problems whose life was saved because after 15 years of misdiagnosis and wrong treatment, a doctor finally decided to think outside the box. Dozens of doctors, multiple hospitalizations, numerous psychological assumptions, and everyone missed that her problem wasn’t in her head or her stomach: she was allergic to gluten. Doctors had almost killed her by telling her to eat carb-heavy meals to gain weight – giving her massive doses of precisely the foods that she was allergic to.

I’m not a doctor. I’m a patient. I was only two pages into the introduction when Groopman said the sentence that leapt out at me, after being told to eat easily-digested carbs "the more she ate, the worse she felt." I knew the problem right then. It took the doctors till page 15 to settle on celiac sprue as the proper diagnosis. Why? Because I’m NOT a doctor. I subscribe to B.F. Synhorst’s theory that "Historically, illnesses are attributed to temperament when science lacks, or refuses to seek, answers".  I don’t automatically blame the patient; when the answer isn’t obvious, I think outside the box. I’ve also, as a patient, heard a lot of other patients say "doctors misdiagnosed my problem for years, but when one suggested celiac, I recovered quickly". What made me a better diagnostician than all the doctors this woman saw? I’ve listened to what other patients have told me about their experiences, and I spotted a detail that got lost in the big picture because I’ve heard this story many times before and know how other doctors solved the problem.

Similarly, we’ve all heard doctors say that it’s haaaaaaaard to diagnose CFS. Then why is it that CFS patient support groups can diagnose it with near-100% accuracy? Once again, because we listen. We’ve heard it all before, we know what tell-tale phrases will spring up in a True CFS patient. Some of us studied CFS under the medical care of one of the nationally-recognized experts (and others have read their books till they’re committed to memory); we actually know more than the average PCP about CFS because we’ve immersed ourselves in it since the 1980s.

Groopman writes that medical students are taught "Only after all the data are compiled should you formulate hypotheses about what might be wrong." Unfortunately, if you begin interrupting after just 18 seconds, you can’t possibly have all the data. The doctor who finally correctly diagnosed the patient’s celiac sprue did just the opposite. He asked her to begin at the beginning, the first symptoms, the doctors, the tests, and let her talk all the way through to the end, listening all the way. By doing so, he picked up clues that others missed.  He started fresh, with an open mind, instead of assuming that the prior diagnoses were correct and the only reason treatment wasn't working was because the patient was non-compliant.

William Osler said that if you listen to the patient, he is telling you the diagnosis. I’ve had doctors blame my divorce for symptoms that started years earlier when I was married, but that was ancient history and they didn’t want to listen to it. Faster and easier to blame the divorce, but that leads to misdiagnosis, because they’ve missed the part where "I have never felt right since the virus in 1987", the part that means it’s most decidedly NOT post-divorce depression. Groopman agrees, "If the patient is inhibited, or cut off prematurely, or constrained into one path of discussion, then the doctor may not be told something vital."

Social psychologist Judy Hall observes "The doctor is supposed to be emotionally neutral and evenhanded with everybody, and we know that’s not true." CFS literature is filled with stories of women who were given psychiatric diagnoses while men with the same symptoms were "really sick".

Unbeknownst to each other, a friend and I saw the same doctor; when we compared notes afterward, he had made the same disparaging remarks to each of us about divorced women; he had the notion that every divorced woman is looking for a way to get alimony so she won’t have to work. He may be a good doctor for men, but he’s going to approach every divorced woman with the attitude that she’s out to fleece her husband. The medical group does nothing to ensure that he sees only male patients, so he continues to misdiagnose divorced women, even those who had been the primary breadwinner and didn’t stand a chance of getting alimony from a near-penniless spouse.

Groopman elucidates "Misdiagnosis is different. ... It reveals why doctors fail to question their assumptions, why their thinking is sometimes closed or skewed, why they overlook the gaps in their knowledge. Experts studying misguided care have recently concluded that the majority of errors are due to flaws in physician thinking, not technical mistakes." "As many as 15% of all diagnoses are inaccurate", primarily because doctors "fell into cognitive traps", like the doctor who consciously or un assumes that all divorced women are scheming to get alimony. Groopman observes "The doctor becomes increasingly convinced of the truth of his misjudgment, developing a psychological commitment to it. He becomes wedded to his distorted conclusion. His strong negative feelings about the patient make it harder for him to abandon that conclusion and reframe the clinical picture differently."

And, in fact, without proper treatment, both my friend and I failed to improve, which "proved" to that doctor that the whole problem was we didn’t want to work. He didn’t need to look for any other reason for our symptoms beyond the assumed desire for alimony. When we reported getting progressively worse, he viewed that simply as "proof" that if we couldn’t get him to say we were disabled with our initial symptoms, we were going to exaggerate until we found the level at which he was convinced of our disability.

Unfortunately, both of us had very real medical problems, which really did become worse and caused further physical damage when they were not properly treated, but because he was filtering everything we said through "divorcee wants alimony", he never once considered that we were telling the truth.

My friend, thank God, got to a different medical group in time, and is now back at work. He and other members of his medical group strung me along with empty promises until it was too late for me to make a full recovery.


Sunday, March 25, 2007

Talk Therapy Doesn't Improve CFS

Cognitive Behavioral Therapy -- thought by some to be the "cure" for CFS proved to be a failure in this test.  Patients complained less about their impairments but the actual objectively-measured impairments themselves did not improve.

Proving once again what patients have been saying for years: you can tell us that we are not sick, you can try to make us believe that we are not sick, but in the long run, all the talking and positive thinking does not change the reality, because this is a virus, not a psychological problem, and viruses cannot be cured by talking about your problems.

To tell a CFS patient that their problems are all in their head is as insulting as telling a cancer patient they don't need surgery, just a head-shrinker.

* * *

Source: Journal of Neurology, Neurosurgery, and Psychiatry
        Vol. 78, #4, pp 434-436
Date:   March 21, 2007

[Short report]

The effect of cognitive behaviour therapy for chronic fatigue syndrome on
self-reported cognitive impairments and neuropsychological test performance
Hans Knoop, Judith B Prins, Maja Stulemeijer, Jos W M van der Meer, Gijs
Hans Knoop, Gijs Bleijenberg, Expert Centre Chronic Fatigue, Radboud
  University Nijmegen Medical Centre, Nijmegen, The Netherlands
Judith B Prins, Maja Stulemeijer, Department of Medical Psychology, Radboud
  University Nijmegen Medical Centre, Nijmegen, The Netherlands
Jos W M van der Meer, Department of Internal Medicine, Radboud University
  Nijmegen Medical Centre, Nijmegen, The Netherlands
Correspondence to: H Knoop, Expert Centre Chronic Fatigue, Radboud University
  Nijmegen Medical Centre, P O Box 9011, 6525 EC Nijmegen, The Netherlands;

Received 26 June 2006
Revised 14 November 2006
Accepted 15 November 2006


Patients with chronic fatigue syndrome (CFS) often have concentration and
memory problems. Neuropsychological test performance is impaired in at least
a subgroup of patients with CFS. Cognitive behavioural therapy (CBT) for CFS
leads to a reduction in fatigue and disabilities.

To test the hypothesis that CBT results in a reduction of self-reported
cognitive impairment and in an improved neuropsychological test performance.

Data of two previous randomised controlled trials were used. One study
compared CBT for adult patients with CFS, with two control conditions. The
second study compared CBT for adolescent patients with a waiting list
condition. Self-reported cognitive impairment was assessed with
questionnaires. Information speed was measured with simple and choice
reaction time tasks. Adults also completed the symbol digit-modalities task,
a measure of complex attentional function.

In both studies, the level of self-reported cognitive impairment decreased
significantly more after CBT than in the control conditions. Neuropsychological
test performance did not improve.

CBT leads to a reduction in self-reported cognitive impairment, but not to
improved neuropsychological test performance. The findings of this study
support the idea that the distorted perception of cognitive processes is more
central to CFS than actual cognitive performance.

Abbreviations: CBT, cognitive behavioural therapy; CFS, chronic fatigue
syndrome; CIS, checklist individual strength; CIS-conc, checklist individual
strength-concentration; SDMT, symbol digit modalities task; SIP-ab, sickness
impact profile-alertness behaviour; SOCI, self-observation of cognitive


Chronic fatigue syndrome (CFS) is characterised by severe fatigue, lasting
longer than 6 months and leading to functional impairment. The fatigue is not
the result of a known organic disease or ongoing exertion, and not alleviated
by rest. According to the Centre for Disease Control definition of CFS,
impaired concentration and/or memory is an additional symptom criterion.1 The
level of self-reported cognitive impairments in CFS is high2 and contributes
to the social and occupational dysfunctions of patients with CFS.3

Studies evaluating neuropsychological functioning in patients with CFS with
neuropsychological tests yielded conflicting results.4 Reduced speed of
(complex) information processing is the most consistently found impairment.3
5 6 However, several studies found no cognitive impairments7 and other
studies identified a subset of patients with defective performance.8 9

Fatigue-related cognitions and behaviour can perpetuate CFS.10 Several
controlled trials have shown that cognitive behavioural therapy (CBT) aimed
at these perpetuating factors leads to a reduction in fatigue and

The first hypothesis tested was that CBT for CFS also results in a reduction
of self-reported cognitive impairments. The second hypothesis was that the
neuropsychological test performance of patients with CFS improves after CBT.
Data of two previous CBT trials12 13 were used to test the hypotheses.



The first study from which data were used compared the effects of CBT for
adults with CFS with natural course and support groups12 in a multicentre
randomised controlled trial. Assessments were done at baseline, and at 8 and
14 months. An intention-to-treat analysis showed a reduction in fatigue and
functional impairment after CBT. In two of the three participating treatment
centres, neuropsychological tests were part of the assessments. Consequently,
data from neuropsychological test performance were available for a subset of
233 (78 CBT; 76 natural course; 79 support group) of the total group of 278
patients. The mean (SD) age of this group was 36.8 (10.2) years, 182 (78%)
were female and median illness duration was 41 months. The second study was a
randomised controlled trial comparing CBT for adolescents with CFS13 with a
waiting list condition. A total of 69 patients were randomly assigned to the
conditions. Assessments were done at baseline and at 5 months. The results
showed a greater decrease in fatigue and functional impairment in the CBT
group. Neuropsychological data of 67 patients were available (33 CBT; 34
waiting list). The mean (SD) age of the group was 15.6 (1.3) years, 59 (88%)
were female and median illness duration was 18 months.

Questionnaires assessing self-reported cognitive impairments

Checklist individual strength-concentration

In both studies, the severity of concentration problems over the past 2 weeks
was assessed with the subscale concentration of the checklist individual
strength (CIS) that consists of five items on a seven-point scale. The score
can range between 5 and 35.3 12 13

Sickness impact profile-alertness behaviour

In adults, the self-observed effect of cognitive impairments on daily
functioning was assessed with the subscale sickness impact profile-alertness
behaviour (SIP-ab) of the sickness impact profile.14 The subscale has 10
items, each item is weighed and the score can range between 0 and 777. No
such instrument was available for adolescents.

Self-observation of cognitive impairment

In adolescents, the frequency of cognitive impairments was determined with a
structured diary. Patients rated both concentration and memory impairment
separately on a daily self-observation list four times a day for 12 days
(0=no impairment; 1=impaired). The percentage of concentration problems and
memory problems (both number of assessments with a problem divided by 48
times 100) were added and then divided by two to calculate the mean
percentage of incidents of cognitive impairment.

Neuropsychological tests

Reaction time task

The reaction time task consisted of two subtests, simple and choice reaction
time tasks. Both are described in detail elsewhere.8 15 In a previous study,
the reaction times of patients with CFS were slower than that of healthy
controls on both tasks.8

Symbol digit modalities task

The symbol digit modalities task (SDMT)16 was used in the adult study as a
measure of complex attention. In previous studies, patients with CFS scored
lower than a matched healthy control group.8 9

Statistical analysis

Statistical analysis was performed using SPSS V.12.01. Significance was
assumed at p,0.05. A multivariate analysis of variance was performed with
self-reported cognitive impairment and reaction time as dependent variables
and treatment as fixed factor. Univariate tests and post hoc analysis are
reported if the multivariate test was significant. For the SDMT, a univariate
analysis was performed, as data were available for a subset of 174 patients
as the SDMT was added later to the test battery. In the adult study, the
dependent variables were the change scores at 14 months from baseline and in
the adolescent study, it was at 5 months from baseline. Reaction times were
transformed by a logarithm transformation. For adults, if data at 14 months
were missing and data 8-months post-treatment were available, the second were
used. In all other cases, missing data were replaced with estimates derived
by single imputation (missing variable analysis regression in SPSS with
baseline value as predictor). For significant treatment effects, effect sizes
were calculated.


Nineteen adult patients (8%) had missing checklist individual
strength-concentration (CIS-conc) and SIP-ab post-treatment data. One patient
had missing data on both reaction time tasks at baseline, for 44 (19%)
patients only baseline data and for 30 (17%) patients only a baseline SDMT
score was available. Two adolescent patients had no SOCI scores at baseline.
For 4 (6%) patients the CIS-conc and SOCI at second assessment were missing.
Two patients had no baseline reaction time and for 13 (20%) adolescents the
reaction times at the second assessment were missing.

In both studies, there were more data missing from neuropsychological tests
than from questionnaires as some patients were willing to mail the
questionnaires, but refused to undergo a second neuropsychological

Self-reported cognitive impairments


The multivariate test (Pillai's trace) showed a significant change in
self-reported cognitive impairments (F(4,460)=4.76; p=0.001). The univariate
tests showed a significant effect of treatment on the change in CIS-conc and
SIP-ab (F(2,230)=8.94; p<0.001 and F(2,230)=4.42; p=0.013). Following CBT,
the decrease in CIS was significantly greater than in both the natural course
(p,0.001) and the support group (p=0.001; table 1). There was a significantly
greater decrease in SIP-ab score after CBT compared with natural course
(p=0.004). The difference between CBT and support group failed to reach
significance (p=0.055).


The multivariate test showed a significant treatment effect on self-reported
cognitive impairments (F2,62=5.03; p=0.009). Univariate tests showed that the
decrease in the CIS-conc and SOCI score was significantly larger in the CBT
group (F(1,63)=6.4; p=0.014 and F(1,63)=6.28; p=0.015).

Neuropsychological test performance


There was no significant effect of treatment on either reaction time task
(F(4,458)=0.44; p=0.783). There was no significant treatment effect on the
SDMT (F(2,171)=0.73; p=0.484).

Adolescents Multivariate tests showed no significant treatment effect on
either reaction time task (F(2,62)=0.34; p=0.714).


The hypothesis that self-reported cognitive impairments decrease after CBT in
patients with CFS was confirmed. Only one comparison in the adult study,
measuring cognitive impairments more indirectly, showed an effect in the
expected direction without reaching significance. The results of the original
adolescent study13 already indicated that concentration problems decrease
after CBT. In that study, the concentration problems were assessed with a
single item evaluating these problems retrospectively over a period of 6
months. This assessment can be easily influenced by situational circumstances
and memory biases, which can be prevented by the use of a diary as in the
present study. No support could be found for the hypothesis that
neuropsychological test performance improves after CBT.

A methodological problem is that in a substantial part of the patients the
neuropsychological data of the second assessment were missing. Furthermore,
in our analysis we assumed that dropout occurred at random, whereas patients
may drop out for non-random reasons. We repeated the analyses, but only on
patients who completed both assessments. Again, there was no significant
treatment effect. Our interpretation is that this indicates that improvement
in self-reported cognitive impairments after CBT is independent of the change
in neuropsychological test performance.

A discrepancy between subjectively reported disabilities versus objectively
measured performance is not limited to the current study. Mahurin et al17
found that the objective cognitive functioning of monozygotic twins
discordant for CFS did not differ, whereas the twin with CFS reported more
cognitive impairments. Metzger and Denney18 showed that patients with CFS
underestimated their cognitive performance. In the study by Vercoulen et al,8
most patients with CFS reported concentration and memory problems, whereas
only a small percentage showed an impaired performance. Given the fact that
patients with CFS perceive their cognitive processes as impaired but
underestimate their actual performance, one would expect that an effective
treatment of CFS would lead to a more accurate perception of one's
performance. The results of the present study are consistent with this
prediction. CBT resulted in decreased complaints about cognitive functioning,
but not in a change in performance. This is also in line with the hypothesis
that a distorted perception of symptoms and performance is a crucial element
of CFS.10


The authors thank Theo Fiselier for contributing to the selection of
adolescent patients with CFS, Lammy Elving for contributing to the selection
of adult patients and Ria te Winkel and Lida Nabuurs for assisting in data

Funding: The Health Insurance Council (College van Zorgverzekeraars) funded
the adult CBT study. The Children's Welfare Stamps Netherlands (Stichting
Kinderpostzegels Nederland) and the ME Foundation (ME Stichting) funded the
adolescent CBT study.

Competing interests: none.


Table 1 Estimated treatment effect in change score (95% CI) on the dependent variables
Self-reported cognitive impairments
  Adults                          CBT                      Natural course        Support group
    CIS-conc                      -7.4 (-9.1 to -5.7)+     -2.7 (-4.4 to -1.0)** -3.4 (-5.1 to -1.8)**
    SIP-ab                        -116 (-156 to -76)++     -31 (-72 to -10)**    -61 (-100 to -21)
  Adolescents                     CBT                      Waiting list
    CIS-conc                      -6.8 (-10.5 to -3.5)+++  -0.9 (-4.2 to +2.5)*
    SOCI                          -7.9 (-12.8 to -2.9)1    0.9 (-4.1 to +6.0)*
Neuropsychological test performance
  Adults                          CBT                      Natural course        Support group
    Simple reaction time (ms)      9 (-9 to 27)            -5 (-23 to 14)        6 (-12 to 24)
    Choice reaction time (ms)     -24 (-51 to 3)           -27 (-54 to 1)        -26 (-53 to 1)
    SDMT                           2.8 (0.8 to 4.8)        2.3 (0.2 to 4.4)      4 (2 to 6)
  Adolescents                     CBT                      Waiting list
    Simple reaction time (ms)     -30 (-53 to -8)          -18 (-41 to 4)
    Choice reaction time (ms)     -12 (-29 to 6)           -10 (-28 to 8)
CBT, cognitive behavioural therapy; CIS-conc, checklist individual strength-concentration; SDMT,
symbol digit modalities task; SIP-ab, sickness impact profile-alertness behaviour; SOCI, self-
observation of cognitive impairment.
*  Significantly different from the CBT condition, p,0.05.
**  Significantly different from the CBT condition, p,0.01.
+   Cohen's d based on change within treatment condition=1.3.
++  Cohen's d=0.6.
+++ Cohen's d=0.4.


1 Fukuda K, Straus SE, Hickie I, et al. The chronic fatigue syndrome: a
   comprehensive approach to its definition and study. International Chronic
   Fatigue Syndrome Study Group. Ann Intern Med 1994;121:953-9.
2 Vercoulen JHMM, Swanink CMA, Fennis JFM, et al. Dimensional assessment of
   chronic fatigue syndrome. J Psychosom Res 1994;38:383-92.
3 Michiel V, Cluydts R. Neuropsychological functioning in chronic fatigue
   syndrome: a review. Acta Psychiatr Scand 2001;103:84-93.
4 Cho, HJ, Skowera, A, Cleare A, et al. Chronic fatigue syndrome: an update
   focusing in phenomenology and pathophysiology. Curr Opin Psychiatry
5 Moss-Morris R, Petrie KJ, Large RG, et al. Neuropsychological deficits in
   chronic fatigue syndrome: artefact or reality? J Neurol Neurosurg Psychiatry
6 Tiersky LA, Johnson SK, Lange G, et al. The neuropsychology of chronic
   fatigue syndrome: a critical review. J Clin Exp Neuropsychol 1997;19:560-86.
7 Dipino RK, Kane RL. Neurocognitive functioning in chronic fatigue syndrome.
   Neuropsychol Rev 1996;6:47-60.
8 Vercoulen JH, Bazelmans E, Swanink CM, et al. Evaluating neuropsychological
   impairment in chronic fatigue syndrome. J Clin Exp Neuropsychol 1998;20:144-
9 Van der Werf S, Prins JB, Jongen P, et al. Abnormal neuropsychological
   findings are not necessarily a sign of cerebral impairment: a matched
   comparison between chronic fatigue syndrome an multiple sclerosis. Neurol
   Neuropsychol Behav Neurol 2000;13:199-203.
10 Prins JB, Van der Meer JWM, Bleijenberg G. Chronic fatigue syndrome. Lancet
11 Whiting P, Bagnall AM, Sowden AJ, et al. Interventions for the treatment and
   management of chronic fatigue syndrome; a systematic review. J Am Med Assoc
12 Prins JB, Bleijenberg G, Bazelmans E, et al. Cognitive behaviour therapy for
   chronic fatigue syndrome: a multicentre randomised controlled trial. Lancet
13 Stulemeijer M, de Jong LWAM, Fiselier TJW, et al. Cognitive behaviour therapy
   for adolescents with chronic fatigue syndrome: randomised controlled trial.
   BMJ 2005;330:7481-6.
14 Berger M, Bobbit RA, Carter WB, et al. The sickness impact profile: development
   and final revision of a health status measure. Med Care 1981;19:787-805.
15 Jolles J. Maastricht aging study: determinants of cognitive aging. Maastricht:
   Neuropsychological Publishers, 1995.
16 Stinnissen J, Willems PJ, Coetsier L, et al. Handleiding bij de Nederlandse
   bewerking van de WAIS [Manual of the Dutch edition of the WAIS]. Amsterdam:
   Swets and Zeitlinger, 1970.
17 Mahurin RK, Claypoole KH, Goldberg JH, et al. Cognitive processing in
   monozygotic twins discordant for chronic fatigue syndrome. Neuropsychology
18 Metzger FA, Denney, DR. Perception of cognitive performance in patients with
   chronic fatigue syndrome. Ann Behav Med 2002;24:106-12.

(c) 2007 BMJ Publishing Group Ltd.