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Volume 1, number 2 |
ME
AND CFS
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1st June 1998 |
In April, I chaired an afternoon session on CFS at the Royal College of General Practitioners. There I met Prof. Simon Wessely, who proved that he is not only a most eloquent writer but also an extremely good speaker. Prof. Wessely and I go back a long way and I've always found him to be friendly and interesting. However, his talk confirmed that he still does not acknowledge the existence of sensible patients with CFS; the type I've seen and the ones described in articles by Drs. Dowsett, Shepherd, Macintyre and other 'ME' specialists.
At the moment, Prof. Wessely believes that CFS is largely maintained by the patients' unhelpful beliefs about exercise and their tendency to avoid all activities associated with fatigue. Change these, he says, and you're halfway there! Sadly, he still refuses to accept that many patients do not have unrealistic views and that there's virtually no evidence that most engage in 'excessive rest'. Nor does he acknowledge that other colleagues see patients who are far more sensible than his, which is why he hasn't mentioned their views and research in his articles and books.
Another development of note is the slight shift away from graded exercise - where one has to keep to a predetermined plan and increase activity levels irrespective of fatigue - towards what might be seen as a mixture of graded activity and pacing. If I have understood correctly, the new advice means you must increase activities as planned but you can stay at the same level if you're unwell. However, unlike the more conventional form of 'pacing', you can't actually go back a stage or even stop.
Personally, I don't know of any ME patients who can sustain their activities when they feel ill, nor incidentally, do I know many who can increase their activities at predetermined levels, for very long. But as I said at the conference, I obviously see a different type of patient!
In the UK, Prof. Wessely's views continue to dominate the journals. For instance, the BMJ carried an editorial written by Sharpe and Wessely with the subheading 'rest has no place in treating chronic fatigue' (1998, 316, 796). I'm sure that you're familiar with the argument: patients take 'excessive rest' and this is the main source of chronic fatigue.
Regular readers of this update already know my position on this. In short, I believe that the current obsession with the 'F' word is still leading to an overly simplistic approach to CFS. For example, are we really to believe that symptoms like cognitive dysfunction and intolerance to alcohol are due to 'excessive rest' and/or strange ideas? If so, why are patients impaired on only some mental tasks and not the whole lot?
Below are some notable findings which adherents to the CBT model may find difficult to explain.
1. Despite what the theory says, patients deal with their illness in different ways, (e.g. Ray et al. Psychosomatic Medicine, 1995, 25, 937, Heymans, Journal of Psychosomatic Research, 1998, 45, 39-51). There's no uniform response to CFS, just as there is none to breast cancer or MS. Recent articles by Wessely and his colleagues have acknowledged a second strategy (excessive rest followed by bursts of activity), but there's still no mention of the more sensible approaches used by many patients (e.g. gentle activity plus adequate rest).2. The next part of the theory, i.e. that fatigue is directly linked to inactivity, also has little support. Jason et al have just published a study (Psychological Reports, 1997, 81, 1223- 1226) where they used a variety of tests for six days to measure fatigue and activity in a patient with CFS (CDC criteria '94). They found that activity was not directly related to fatigue! To put it another way, this person did not reduce his activity just because he was tired. Admittedly, this study only assessed one patient and it would have been more useful if they had measured other symptoms as well. However, it fits in with the anecdotal reports, and with previous research. In short, there's a whole lot more to CFS than fatigue and it saddens me that my psychiatric colleagues are still not taking this on board.
3. There's also other evidence undermining the view that inactivity is the main source of chronic fatigue. Lane et al looked at the structure of muscle cells and the response to exercise in 105 patients with CFS (Oxford criteria, Journal of Neurology, Neurosurgery and Psychiatry, 1998, 64, 3, 362-367). A proportion of patients had abnormal biopsies though there were no consistent changes. In addition, 37% had abnormal lactate responses to exercise. However, the changes in the muscle tissue were not like those "expected as a result of inactivity" and the researchers also dismissed the idea that a lack of exercise alone had resulted in the abnormal lactate levels.
4. Wessely and colleagues have claimed that conventional advice to 'accommodate to the illness' (i.e. pacing) is likely to make patients feel worse. However, Knussen and Lee (British Journal of Health Psychology, 1998, 3, 111-121) found that people using this strategy actually had fewer symptoms than those who used other ways of coping. They were also less likely to perceive the illness as stressful, to experience more optimism and to perceive that the illness had a less negative impact. Perhaps psychiatrists should be reminded that pacing is not another word for focusing on your symptoms and worrying (cf. Update, 20th May 1998).
5. Wessely and colleagues continue to argue that the persistent virus theory can now be dismissed. However, Miller et al have just reported that they found CD45RO memory T cells in the spleen of a patient with CFS. According to a knowledgeable consultant, this is significant because one would not expect these cells to congregate in the spleen unless they were signalled by an infection, virus etc.
6. Although he wrote something different in his book, Prof. Wessely now accepts that views about the causes of CFS ('attributions') are NOT a major influence on recovery (Update, 1998, 20th May). The latest findings which support this stance come from a follow-up study by Ray et al (Journal of Psychosomatic Research, 1997, 43, 4, 405-415). Other variables which did not affect the course of the illness included depression and anxiety. Meanwhile, Heijmans (see above) found that a belief in a biological cause was related to fewer mental health problems while a belief in a psychological cause was associated with the opposite. Moreover, a belief in a biological cause did not, as the CBT model predicts, lead to widespread avoidance.
The fact is that as an archivist, I can't think of any sound evidence which supports the CBT model. If there was, I'd let you know. On the basis of the research alone, I remain of the opinion that this theory is still unproven and unrealistic. As for the changes in emphasis, I don't consider the newer version as an improvement on what went before. We seem to have gone from the superwimp* theory, which implied that patients are afraid of fatigue, to the fruitcake* theory, where all patients have strange and unhelpful beliefs (see Update, 1998, 20th May for examples). Basically, doctors are being presented with a caricature, and I for one, find this difficult to accept.
Instead of focusing on what patients think about activity (we know that now), researchers should determine when they should exercise and when they should rest. British psychiatrists argue that patients should stick to a plan more or less, irrespective of fatigue. American psychologists believe that most may do better if they match exertion and energy. Watch this space to see which advice is better and for whom!
A new trial of graded exercise etc., revealed only modest improvements. (NB. New trials all include some type of heart monitoring. My advice: do not start a graded exercise programme without it!) Secondly, a study by Prof. Wessely's team showed that beliefs about the causes of CFS "are less important in determining outcome than previously thought" (J. Psychosom. Res., 1998, 45, 77-83). Finally, Sisto et al measured activity levels for two weeks and confirmed that CFS patients do not spend all their time engaging in 'total rest'. They also reported that exercise did not lead to a major reduction in activity, which the CBT theory predicts (Quarterly Journal of Medicine, 1998, 91, 465-473).
When I started speculating about subgroups and writing about fatigue syndromes, I was pretty much on my own. Now, expert after expert seem to be saying the same thing. The latest convert is influential psychiatrist Dr. Mark Demitrack. He was recently asked by CFS-NEWS to comment on one of the papers on cortisol. (Demitrack et al. published a well known study in 1991 that indicated that cortisol levels were lower in CFS patients, the opposite of the findings by Wood et al.) Trying to explain the inconsistent results, he said: "We are now well aware that the population of individuals defined by the traditional criteria used to specify a case of CFS probably encompasses an etiologically heterogeneous group of people." In other words, we're dealing with a number of different causes. To remind you, the CBT model mentions the heterogeneity of the patient population but doesn't take it into account.
Copies of the listed articles can be obtained though your local library.
Sometimes the referees who assess papers seem to overlook some most peculiar findings. Take the results of an epidemiological study by Wessely et al (American Journal of Public Health, 1997, 87, 1449). They found that 2.6% of their patients fulfilled the CDC criteria from 1994 but that 2.2% met the much broader, i.e. less restrictive Oxford criteria. Of course this doesn't make any sense but it wasn't anything that bothered the referees.
Another anomaly can be found in the increasingly unsympathetic British Journal of Psychiatry (1997, 171, 377). It concerns a report by the well-known Australian research team headed by Andrew Lloyd and Ian Hickie. Having selected their patients using out-dated criteria is one thing. However, what really caught my eye was that they found the fatigue scores of their CFS group to be below those of patients with depression or acute infection. This is really a first, as far as I can tell. To date, all the research has shown that the fatigue in CFS patients exceeds that of other people. So what happened here? Were the patients tested when they were well? If so, are the results typical for CFS? If not, why did the referees not ask for an explanation? Let's hope that this is not another case where they liked the results so much (no difference in cognitive performance between CFS and depression) that the flaws were overlooked.
Copyright EM. Goudsmit 1998.
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