Terms Physical
attribution: a belief in a
physical cause. Deconditioning: loss of
physical fitness. CBT: cognitive-behavioural
therapy. Graded
exercise: activities are
increased according to a predetermined plan. Patients cannot
take a step back or stop when ill. Pacing: Activity is
linked to how a person feels that day. The aim is to avoid
overexertion and relapse.
According to the CBT model described by Sharpe, Wessely and Vercoulen, physical attributions lead patients to reduce their activity levels, which in turn increases deconditioning and perpetuates the fatigue. It follows that increasing activity will reduce deconditioning as well as fatigue. The proponents of this theory also claim that looking for causes is futile and may prevent recovery. Depression further exacerbates fatigue.
There is no evidence that every patient with CFS adheres to one and the same attribution. Research suggests that people generally have more sophisticated views (e.g. Ware and Kleinman 1992, Ray et al 1992, Goudsmit 1996 etc.).
Physical attributions may be accurate and changing them would be inappropriate! See the growing evidence of immune activation, increased antibodies of certain viruses, etc. (e.g. Lerner et al, Cannon et al 1997). This possibility is rarely mentioned in the literature on CFS.
Adhering to a physical attribution does not stop patients trying non-somatic forms of treatments as claimed by Vercoulen, hence the low refusal rates for trials of CBT etc.(Sharpe et al 1996, Fulcher and White 1997).
Adhering to physical attributions did not predict ongoing fatigue in two longitudinal studies (Lawrie et al 1997 and Ray et al 1997), nor did it prevent recovery in people trying CBT (Bonner et al 1994). The association between physical attributions and poor outcome (by Sharpe et al 1992) relates to variables measured at the same time; one did not predict the other. Those with a poor outcome were also more likely to report intolerance to alcohol. The findings therefore probably describe a subgroup of severely ill patients. The only other finding of a link between physical attributions and poor outcome relates to a very mixed group. Again, the people who believed they had a physical illness may have represented a subgroup who were more severely ill. Interestingly, articles don't generally mention this interpretation of the findings!
Wessely's own team found that physical attributions were not associated with a poor outcome (New research by Deale et al. J. Psychosom. Res., 1998, 45, 77-83).
Reducing activities is a coping strategy which people use partly because it appears to reduce symptoms (Clements et al 1997). Patients following the conventional advice to keep within their limits and avoid overexertion tend to improve (Goudsmit 1996, King et al 1997) and there is no evidence of poor outcome except for those with a low internal locus of control (Ray et al 1997) or a pessimistic, passive attitude (Heijmans 1998).
In general, the level of activity among CFS patients is the same as that found in people with MS (Vercoulen et al 1997).
Another study revealed that CFS patients spent only 16.8% of their daytime hours resting (Packer et al 1997).
'Inactivity' does not lead to CFS symptoms in other sedentary groups, e.g. those recovering from a broken leg, prisoners etc.
'Inactivity' does not explain cognitive deficits, intolerance to alcohol, sore throats, vertigo and the other less publicised symptoms of CFS.
'Inactivity' does not explain some of the muscle function abnormalities which have been found (e.g. Lane et al. 1998). Indeed, activity while ill may affect ongoing disease (e.g. Lapp 1997, McGarry et al 1994, Miller et al 1998).
Lack of stimulation would produce global impairments in cognitive function, not the specific ones documented to date (e.g. Marcel et al 1996, De Luca et al 1997). It seems that the role of inactivity may have been exaggerated.
A study by Heijmans among members of the Dutch ME Association found that a view in a biological cause was not associated with avoidance. Moreover, avoidance of activities did not predict physical functioning, social functioning, mental health or vitality. In short, there is little support for the CBT model and its prediction that physical attributions will inevitably lead to the avoidance of activities and a perpetuation of fatigue.
Prof. Wessely recently suggested that beliefs about exercise might be more important in determining avoidance than attributions about causes (Deale et al 1998). His research assessed four beliefs. While some were associated with a poor outcome (e.g. 'I should avoid exercise when tired'), at least one was not ('exercise is harmful').
The majority of patients with CFS do not have a history of major depression, and rates of current depression generally resemble those of patients with MS or cancer (Goudsmit 1996). Depression is different from, and cannot explain CFS (Vercoulen 1997). The same is true for anxiety.
Further tests to identify additional disorders can improve treatment and reduce disability (Teitelbaum and Bird 1995). They are therefore not 'futile'.
Recent successful trials of graded activity (e.g. Wearden et al 1998) have all used heart monitoring to avoid overexertion. Experts now rarely insist on increases in activity when patients are unwell, though 'graded' implies that individuals cannot reduce or even stop. This is not always mentioned though. Having reviewed the literature and talked to colleagues, there appears to be a trend towards towards pacing, which is more suitable and appropriate for patients without comorbid psychiatric disorders and personality problems.
Many rehabilitation programmes include not just CBT and graded activity, but also dietary advice, supportive counselling and massage (Essame et al 1998). It's inaccurate to describe these as CBT/graded exercise.
There must be a subgroup of CFS patients whose attitudes and behaviour fit the descriptions by Wessely, Sharpe et al. For them, CBT and graded exercise is probably the treatment of choice.
NB. As an archivist, I get the impression that research using the Oxford criteria tends to select more patients with psychiatric and personality disorders than the stricter CDC criteria. It should also be noted that all the positive reports about graded exercise have come from the UK. Studies outside Britain (which probably selected a different population) have been disappointing.
If viral infections trigger CFS and attributions maintain it, when does the switch occur? At six weeks, six months? Why are perpetuating factors (primarily attributions and inactivity) causing exactly the same symptoms as the initial infection did before there was any physical deconditioning?
Why should a whole group of people react in the same uniform way to viral infections? Other patient groups do not respond to their symptoms in the same way!
60-80% of patients with acute onset post-viral CFS improve over time without changing attributions or using graded exercise (e.g. Goudsmit 1996, Lerner et al 1997). About 80% feel better after treatment programmes including rest and pacing, so CBT and graded exercise is not the only effective intervention.
Why is there an assumption that all scientists who support a non-psychiatric explanation suffer from attributional bias? Are all those who favour the CBT explanation unbiased?
Why are some researchers testing the CBT model now excluding patients with PVFS from their trials (e.g. Sharpe et al 1997)?
Finally, note the complete monopoly of the CBT school in the British medical journals. I don't recall any researcher from outside this school publishing anything in a mainstream British journal lately. How can we conduct a sensible debate about the research if all those with different views are excluded? (cf. Royal Colleges Report 1996).
Cognitive behaviour therapy (CBT) is based on the cognitive behavioural model of chronic fatigue syndrome. The latest description, by Chalder et al 1996 is printed below. I've used their words so that I cannot be accused of misrepresentation. However, to save space, I've omitted the references and one or two descriptions of research.
"The literature suggests that the premorbid personalities of patients with CFS are characterised by a marked hyperactivity or workaholism and achieve-ment orientation, perfectionism and high standards for work performance. Patients' pre-illness lifestyles have typically consisted of prolonged striving in order to achieve the personal high standards they have set for themselves. Failure to meet these standards results in the person feeling dissatisfied. Achievements seem to have an all or nothing quality about them and patients report an inability to enjoy whatever they are doing unless they are doing it well. These harsh personal expectations place an enormous burden on the individual, so much so that when an acute illness is experienced and the person is unable to perform to the usual high standard, he/she believes that something must be wrong.
Set in this context, delayed recovery from an infection, for example, may be the "straw that breaks the camel's back". Although there is little evidence that common viruses can cause a chronic fatiguing illness one recent study showed an association between Epstein Barr virus and delayed recovery six months after onset. It is likely, however, that once several years have past, factors other than the virus would be influencing the pattern of symptoms.
At the time of infection it is pertinent to rest in response to symptoms of fatigue, but if the patient is still fatigued and resting six months later, then it is reasonable to consider the contribution of factors other than the initial virus in the continuing illness.
Why might patients be resting six months after the onset of the symptoms? People generally use rest as a strategy for reducing symptoms. However, in some a reduction of symptoms does not occur. The symptoms persist and the person, understandably, continues to rest. Slowly, a reduction and avoidance of activities takes place for fear of bringing about a worsening of symptoms...
A number of studies have demonstrated that making physical illness attributions for fatigue predicts degree of disability in patients with CFS... Many patients may believe the viral infection that triggered off the illness in the first place is a persistent one, and that this accounts for their ongoing fatigue. As viruses are potent, uncontrollable, aversive, frightening and untreatable, feelings of being out of control are experienced. This can be compounded by the advice given to sufferers. Some patients believe, and have been told, that they have a neuromuscular disease. Consequently, they worry about the risk of causing further muscle damage. This is an understandable response to the presence of myalgia, but it may not be an accurate attribution. Although some studies have suggested muscle abnormalities in CFS, the general consensus is that neuromuscular function is normal in sufferers.
A further cognitive factor in CFS is that many patients, in an effort to control and reduce symptoms, often by adjusting activity levels, become hypervigilant and over-sensitised to bodily sensations. This `symptom focusing' may serve to exacerbate unpleasant sensations and has been shown to be associated with fatigue in patients with CFS.
In summary then, symptoms are perpetuated by physical illness attributions, unhelpful cognitions and schemas relating to perfectionism and avoidant coping strategies".
Deale, A., Chalder, T., Marks, I and Wessely, S. Cognitive behaviour therapy for chronic fatigue syndrome: a randomised controlled trial. American Journal of Psychiatry, 1997, 154, 3, 408-414.
This trial compared the effectiveness of CBT and graded activity (CBT) with a programme consisting of relaxation training (e.g. progressive muscle relaxation, visualisation). All 60 subjects fulfilled the Oxford guidelines and CDC criteria ('92 and '94).
Before the 13 sessions of treatment, there were no significant differences between the two groups except for age. However, there were some non-significant differences: duration of illness (3.4 years in the CBT group versus 4.6 years in the relaxation group), use of antidepressants (13% in the CBT group versus 27% in the relaxation group). In the CBT group, 57% attributed their symptoms to physical illness compared with 73% of the relaxation group.
Effectiveness was measured using the MOS-short form which assesses disability, the fatigue questionnaire (Chalder et al 1993), the General Health Questionnaire (GHQ)-12 and the Beck Depression Inventory (BDI). Patients were also given a psychiatric interview to determine their psychological status. Assessments occurred pre, during and post treatment, and 1, 3 and 6 months afterwards. The drop out rate was low (n=7).
Scores at completion of treatment revealed the greatest group differences for the assessment of the patients' 'long-term goals'. There were no differences on the fatigue questionnaire, GHQ or BDI.
At final follow-up, 70% of the CBT group achieved good outcomes, as did 19% of the relaxation controls. There were substantial improvements in physical functioning, work and social adjustment (MOS-short form) and fatigue. In contrast, there were no significant changes on the BDI or GHQ. Thirty per cent of the CBT group rated themselves as unchanged or worse compared with 69% of the controls.
Neither psychiatric status nor attributions appeared to affect outcome. As to satisfaction with treatment, 78% of the CBT group were satisfied or very satisfied compared with 50% of the patients in the control group.
In my view, the results are difficult to interpret because:
1. There are no details regarding the history of infection and the proportion of patients with an acute or gradual onset (see Reyes et al 1997).
2. There are no details about the presence of and effect on symptoms other than fatigue and depression.
3. The groups were not evenly matched before treatment (see above) although differences were not statistically significant. There is some evidence that the controls may have been slightly more disabled than the patients receiving CBT.
4. The improvements in levels of fatigue showed at 6 months follow-up but not after completion of the treatment. This is baffling? Why should CBT begin to benefit patients after the course is finished.
5. Progressive muscle relaxation is likely to make people with ME worse. This could partly explain the poor results of the controls.
6. Since fatigue syndromes like ME fluctuate, about 50% of the patients should have improved regardless of treatment. However, the controls didn't. Some were worse off than they might have been had they remained on the waiting list.
7. A 70% improvement is not impressive. In other studies, evening primrose oil helped 80% and magnesium injections helped about 80%. Even Royal Jelly helped 69%.
8. Why did 30% remain unchanged or get worse on CBT? Were these the most severely affected, those with an infectious onset, those with ME?
Chalder, T., Butler, S and Wessely, S. In-patient treatment of chronic fatigue syndrome. Behavioural and Cognitive Psychotherapy, 1996b, 24, 351-365.
This paper describes the treatment of 6 patients who fulfilled the criteria for CFS (not specified) and who thought that they had myalgic encephalomyelitis (ME). Five cases followed a viral infection and all were members of the ME Association.
All except one of the patients fulfilled the criteria for major depression. Some had additional diagnoses including phobic anxiety and somatisation disorder. The person who did not suffer from major depression fulfilled criteria for minor depression.
Patients were admitted to a neuro-psychiatric ward for three to eight weeks. Mean therapist time was 10.5 hours. After discharge, patients were seen at four out-patients appointments. Care was taken to establish an accepting empathic relationship and a list of realistic and acceptable targets was drawn up. Patients were not asked to increase activity levels until the previous activity could be performed without undue physical difficulty. A record of activities and symptoms was kept for later discussion. Planned rest, an important part of the programme, was also regulated, taken at set times and for set duration’s rather than in response to symptoms. The emphasis was placed on breaking the association between experiencing symptoms and stopping activity. The patients were also asked to monitor negative automatic thoughts and to generate more helpful alternatives. They were informed that setbacks were inevitable and instructed how these should be dealt with. In two instances, relatives were asked to act as co-therapists. Five patients were given anti-depressants (dothiepin 50-150 mg daily).
The results indicated substantial improvements in five cases. There were reductions in fatigue and depression and improvements in work and social functioning. Four of the patients maintained these improvements at three months follow-up and two were able to return to work. One person discontinued treatment at discharge.
The researchers state that it is unclear whether recovery was related to therapist time, specific techniques or anti-depressants.
These patients all suffered from depression, a condition known to respond well to CBT. I would have liked to have seen details of immunological tests to know if these patients actually had evidence of persistent infection e.g. to Epstein-Barr virus, cytomegalovirus, HHV-6 and 7 and other viruses linked with CFS. A recent study which focused on subgroups of CFS found that patients who had elevated levels of antibodies to cytomegalovirus benefited from the anti-viral drug ganciclovir (Lerner et al, Infectious Diseases in Clinical Practice, 1997, 6, 110-117).
In my opinion, British researchers must now start to differentiate between the various subgroups as recommended by American and Australian authorities (including the respected CDC). If we don't, we're not going to identify exactly which patients respond to which treatment. What we are doing at the moment is the equivalent of taking 100 patients with recurrent headaches, finding that the majority are helped by aspirin, and forgetting to assess the minority who don't. In my view, this means that many patients are not getting the specialised help they need and deserve.
To recap, the rationale for CBT/planned activity is that CFS is the result of three problems: inactivity, physical attributions and depression. The theory is that fatigue leads to inactivity ('total rest') which increases deconditioning and exacerbates fatigue; this and a belief that the illness is viral and therefore incurable induces hopelessness; the latter results in depression and further fatigue. According to the King's College team, the persistence of CFS is therefore the result of psychosocial factors, not biological ones.
My doubts about CBT emanate from the fact that neither the theory nor the descriptions of CFS patients who took part in the trials fit my clinical experience of ME, or the case histories I have read in the medical journals, or some of the research I have studied and written about during the past 13 years. It's as though most of the patients consulting the CFS clinics in Oxford and King's College constitute one specific subgroup. Or have I, and the other ME specialists been the ones who have seen the less typical cases?
A few more thoughts. Study 1 shows that depression does not affect outcome and that a 'physical' attribution does not inhibit recovery. So if these factors are irrelevant, we're left with inactivity as a major cause of CFS. This leads us to the following questions:
1. does inactivity alone lead to the perpetuation of CFS and2. is CBT combined with planned activity the best treatment.
The answer to the first question seems to be no. There has not been a great deal of research on activity levels but what has been published so far has failed to show a strong relationship between inactivity and fatigue in CFS. The answer to question 2 is probably also no. Pacing activity i.e. not ignoring symptoms but staying within one's limits led to improvements in 80% of patients with post-infectious fatigue (research by Drs Goudsmit and Ho-Yen). So the specific advice to push on and stick to a plan is not essential for successful treatment. Kindness, support and practical tips may be much more important.
Study 2 shows quite clearly that ME patients who also suffer from clinical depression benefit significantly and quickly to CBT and planned activity. This supports earlier findings by Friedberg and Krupp. Therefore my updated advice to CFS patients who are also suffering from mood disorders, and to anyone whose experience fits the description of sufferers by Chalder et al (1996b) is now as follows:
Accept that psychological problems can delay your recovery, so be honest with yourself and accept CBT if it is offered to you. You could be much improved within 6 months.
As for the patients with infection-related CFS who are still mobile, who are not depressed and who do not have the personalities described above, there is still no evidence that CBT/planned exercise is particularly helpful. Would I try it anyway? To be honest, no. I'd begin a healthy, low-sugar diet, I'd ask for symptomatic treatment for symptoms such as insomnia, nausea, pain or depression, I'd find myself a sympathetic psychotherapist or counsellor to support and guide me during this difficult period, I'd balance activity and rest (advice Ho-Yen/Jason et al) and I'd try to retain a positive (optimistic) outlook. This approach resembles CBT in many ways but it is not based on a highly simplistic theory and does not require patients to ignore their intuition and experience.
Ellen Goudsmit PhD C. Psychol.
Editor ME and CFS Capita Selecta Quarterly
There have been three trials of graded exercise: two have been published, one was described at a recent conference.
The following points should be noted:
The trials published to date involved patients whose tiredness appears to be related to maladaptive beliefs plus inappropriate inactivity (i.e. related to fears, not symptoms). These are not sensible patients who use pacing and the more common strategies.
The trials to date included some form of heart monitoring. This is important, e.g. Lapp. One should not dabble in 'graded exercise'.
The third trial by Campion et al (reported in GP 10.4.98) found graded exercise/CBT to be ineffective. This may be because the population tested was different from the above or because the GPs did not have the skills and/or time required.
A recent report by Dr. Mike Sharpe suggests that some of the improvements seen in the short-term may not last. In the Linbury Research Portfolio on Chronic Fatigue (ed. R. Fox), Sharpe writes that "CBT is rarely curative" and "a proportion slip back" (p. 61).
See also White, PD and Naish, VAB. Graded exercise therapy for chronic fatigue syndrome. Physiotherapy, 2001, 87, 6, 285-288.
Fulcher, KY and White, PD. Randomised controlled trial of graded exercise in patients with the chronic fatigue syndrome. British Medical Journal, 1997, 314, 1647-1652.
This trial assessed the efficacy of a graded aerobic exercise programme for patients with CFS. Sixty-six patients with CFS (Oxford criteria) who had neither psychiatric disorders nor appreciable sleep disturbance, were randomly assigned to receive 12 weeks of either an exercise programme or flexibility treatment with relaxation. Patients who completed the latter were allowed to cross over to the exercise programme afterwards. Median duration of illness was 2.7 years.
Measures included the Hospital Anxiety and Depression Scale (HAD), the fatigue questionnaire (Chalder et al 1993), the Pittsburgh Sleep Quality Index, the MOS short form and self rated impression of global change. In addition, patients were assessed using a treadmill walking test to determine their peak oxygen consumption, perceived exertion, heart rate and thumb prick lactate concentrations. The follow-up after three months included a psychiatric interview and self-rated global impression change.
The exercise treatment included laboratory sessions and exercise at home, five days a week, starting at an intensity of 40% of peak oxygen consumption. This increased by one or two minutes up to a maximum of 30 minutes. The intensity of the exercise was then increased to 60% of peak oxygen consumption. Patients were advised not to exceed the prescribed levels during good periods. They were also given heart rate monitors to ensure that they did not exceed target heart rates. If fatigue increased, patients were advised to remain at the same level of exercise for an extra week and increase only when the fatigue had lessened.
Flexibility treatment involved stretching exercises and relaxation techniques starting off at ten minutes and increasing up to 30 minutes. They were also asked to avoid doing any extra physical activities. Patients kept a weekly diary to record type, duration and response to exercise which determined their next week's prescription.
Ten patients were taking normal dose antidepressants and 10 were taking low-dose tricyclics as hypnotics. Forty-four patients blamed viruses for their illness. Seven people dropped out of the trial.
Following treatment there were improvements in median peak oxygen consumption, especially after exercise. There were also improvements in isometric strength, and less perceived exertion on the treadmill test. However, these measures were not related to the global improvement scores.
In the exercise group, 16 out of 29 patients (55%) reported being "much better" or "very much better" compared with 8 of the 30 (27%) patients in the flexibility group (p=.05). Six per cent were unchanged or a little worse in the exercise group as were 10% of the flexibility group. At three months follow-up, 32 out of 47 (68%) patients (including the cross-over ones) felt better. At 12 months, 35 out of 47 (74%) rated themselves as better on a questionnaire. Several people in the exercise group had returned to work or study at least part time (66% compared with 39% prior to treatment).
Total fatigue, physical functioning and general health were found to have improved at completion of the treatments and particularly after exercise. For example, the fatigue score in the exercise group fell from 28.9 to 20.6 after 12 weeks (14 is "normal" score) and the physical functioning score increased from 48.5 to 69 (mean for general population is approx. 84*). However, there were no significant differences for mental fatigue, depression and anxiety.
The researchers note that exercise treatment seems to work more quickly than CBT-based programmes as 52% of the patients had improved (by intention to treat analysis) after three months compared with 27% at five months after CBT (cf. Sharpe et al 1996). Comparison between the trials is difficult, however, because the samples used were different. "These findings support the use of appropriately prescribed graded aerobic exercise in the management of patients with the chronic fatigue syndrome".
[Ed. note: the paper does not mention how many patients had a sudden or gradual onset, or any symptoms other than fatigue, anxiety and depression. The reason for the use of therapeutic dosages of antidepressants by the patients who were not depressed is not given. *This statistic is taken from Komaroff et al, Am. J. Med, 1996, 101, 281.]
Wearden, AJ., Morriss, RK., Mullis, R., Strickland, PL., Pearson, DJ., Appleby, L., Campbell, IT and Morriss, JA. Randomised, double-blind, placebo-controlled treatment trial of fluoxitine and graded exercise for chronic fatigue syndrome. British Journal of Psychiatry, 1998, 172, 485-490.
Patients with CFS (Oxford criteria), of whom 46% had current psychiatric disorders were randomly assigned to four groups:
1. n=33 graded exercise plus fluoxetine (20 mg),2. n=34 graded exercise plus drug placebo,
3. n=35 exercise placebo (exercise when able, rest when needed) plus fluoxetine,
4. n=34 exercise placebo plus drug placebo.
Drop outs from each group were as follows:
1. 142. 11
3. 10
4. 5
The drop-outs tended to be more severely impaired (MOS).
Graded exercise in the trial involved patients doing their preferred aerobic activity e.g. walking, jogging, swimming or cycling for 20 minutes, three times a week. The initial intensity was set at a level which utilised about 75% of the subject's tested functional maximum. Subjects monitored their programmes using a chart, heart-rate (measured pre and post exercise) and the perceived exertion scale (PES). Activities were increased when there was a consistent recorded reduction in heart rate (10 beats per minute) in post-exercise HR for one week and two points on the PES.
Measures included the fatigue scale (Chalder et al 1993), MOS-SF, HAD and a psychiatric interview (CIS-R). The physiological assessments included functional work capacity which was determined using a braked cycle ergometer and was calculated as the amount of oxygen consumed in the final minute of exercise per kilogram of body weight. All patients also kept special diaries which were discussed with the physiotherapists every four weeks.
Subjects were assessed at baseline and after 12 and 26 weeks. The contact with the physiotherapist was on weeks 0, 1, 2, 4, 8, 12, 20 and 26. Twenty-six per cent of subjects were members of self-help groups. Seventy-one per cent of the total sample completed the trial.
Graded exercise improved functional work capacity but not fatigue. Fluoxetine led to a reduction in depression scores at week 12.
In trial completers only, there was a significant improvement on the MOS health perception scale at 26 weeks but not at 12. There was also a significant improvement in fatigue scores both at 12 and 26 weeks with a 12% reduction in patients with case level fatigue (score >4) by 26 weeks. There was also a 10% reduction in functional work capacity at 12 and 26 weeks. Exercise did not improve depression.
Of the 21 drop-outs assessed at 26 weeks, there was no worsening of fatigue, functional work capacity, MOS health perception or depression.
The researchers suggest that graded activity may provide patients with reassurance that exercise at a controlled rate need not exacerbate fatigue.
With commentary by Deale, A., Chalder, T and Wessely, S (p. 491-492.) This notes the "modest" effects, which they attribute to behaviour change as a result of which there was a cognitive shift away from fear and avoidance. They add that more attention should be paid to the overlap of CFS and atypical depression with a view to assessing the effectiveness of MAOIs. Finally, it is possible that 20 minutes was too much for some patients and that a more flexible programme could have produced a better outcome.
Paul, L., Wood, L., Behan, WMH and Maclaren, WM. Demonstration of delayed recovery from fatiguing exercise in chronic fatigue syndrome. European Journal of Neurology, 1999, 6, 63-69.
(Objective evidence of muscle dysfunction)
Sisto, SA., Tapp, WN., LaManca, JJ., Ling, W., Korn, LR., Nelson, AJ and Natelson, BH. Physical activity before and after exercise in women with chronic fatigue syndrome. Quarterly Journal of Medicine, 1998, 91, 7, 465-473.
(Includes objective measure of activity and the results challenge the CBT theory of avoidance and 'total rest').
Lovell, DM. Chronic fatigue syndrome among overseas development workers: a qualitative study. Journal of Travel Medicine, 1999, 6, 16-23.
(This group of patients showed no sign of adhering to a single maladaptive attribution and did not respond to fatigue with avoidance or depression.)
Copyright EM. Goudsmit, PhD C.
Psychol. 1998. ©
Editor ME and CFS Capita Selecta Quarterly
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Professor Simon Wessely and his team have produced a web-site "Chronic Fatigue and Chronic Fatigue Syndrome - A Practical Self Help Guide".
Information on chronic fatigue and CFS from researchers and clinicians who favour a cognitive-behavioural explanation. The account of CFS does not acknowledge the evidence favouring alternative views, or the suggestion that ME is a subset of CFS (broadly defined). The updated advice on activity has similarities to the method described by patient groups as 'pacing', and there are additional tips for people whose fatigue is perpetuated or exacerbated by social and/or psychological problems.
