In 1988, doctors advising the American Centres for Disease Control (CDC) formulated a working case definition for a disorder they called chronic fatigue syndrome (CFS). It was thought to be a single illness, probably the result of infection, but not as 'neurological' as the established condition known as myalgic encephalomyelitis (ME). Unfortunately, the criteria for CFS actually selected a mixed population and now this term covers nearly everyone with profound, chronic, unexplained fatigue1. For instance, in articles published here and in the States, it has described cases of fatigue due to primary sleep disorders, simple nutritional deficiencies, stress and a number of psychiatric conditions. Another subgroup is ME. This can be summarised as a post-viral syndrome where the fatigue is closely linked to exertion, and where other symptoms suggest impaired circulation and central nervous system involvement. It's similar, though not identical, to some cases of fibromyalgia and Gulf War syndrome.
Prevalence studies support this analysis. A study using the latest criteria estimated that about 2-3% of the general population may have CFS. Conversely, criteria used to identify ME-type syndromes select a much smaller population, about 0.1%2. Given the differences which have been found among the various fatigue syndromes, it's no longer valid to describe CFS as a single entity with a single cause3.
Incidentally, CFS has remained a research diagnosis. There are no accepted criteria for use in clinical situations so GP's are still entitled to diagnose post-viral fatigue syndrome, listed as G93.3 under Diseases of the Nervous System in the International Classification of Diseases, volume 10 (ICD-10), or neurasthenia, category F48.0 found under psychiatric disorders4. Although the World Health Organisation no longer recommends the use of the term ME, the current reluctance to diagnose this condition probably has more to do with medical politics and current fashions rather than science or a desire for accuracy.
In my view, the use of increasingly wider criteria and the obsession with fatigue has created much confusion and misunderstanding during the past decade. If one compares the descriptions of the symptoms of ME and CFS, the personalities of the patients and the prevalence rates, one can tentatively conclude that all patients with ME have CFS but that not everyone with CFS has ME.
Almost every illness has a physical and psychological component so splitting disorders into the medical and psychiatric is simplistic to say the least. However, the fact is that many doctors still do not provide the same level of emotional and practical support to those with psychosomatic conditions. Moreover, only people with a physical disability qualify for the higher rate mobility component of DLA in the UK. As we have to deal with the real world and real prejudices, here is some of the evidence for ongoing 'physical' disease.
In broadly-defined CFS, the research is equivocal and confusing. However, studies on more strictly defined groups have identified abnormalities within the brain5,6, muscles7, heart8, and immune system9. Some of these changes have been linked to the severity of the disease10. Less clear are the roles of stealth viruses11, metabolites like CFSUM1 (doubts have arisen since the early research has not been replicated, even by the same team12), mutant enteroviruses13 and the increased rates of cell death14.
In short, there is some evidence for a persistent viral infection in a subgroup of patients, while in others, there are clear signs of immune system activation, muscle damage and other changes suggesting ongoing disease. Studies being completed at the moment are assessing whether low blood volume, the blood brain barrier and presence of certain pathogens (bacteria, parasites) in the gut play a significant role in CFS.
The research suggests that among broadly-defined populations, there is a subgroup whose ongoing fatigue may be the direct result of excessive inactivity and maladaptive (irrational, unrealistic) beliefs15. This subgroup tends not to have the abnormalities discussed above. A small proportion of patients are thought to suffer from a somatisation disorder (i.e. hysteria) or depression which have been misdiagnosed.
Please note that there is as yet no reasonable evidence that this explanation applies to the majority of people with CFS (see update elsewhere).
Since this is such a mixed population, effective management depends on which subgroup one belongs to. For instance, some patients with signs of ongoing infection have responded to the appropriate anti-viral or immunity-boosting drugs8. Where there is a lack of certain vitamins (D, B12) or food sensitivities, supplementation and dietary modification have had impressive results16. Indeed, some American specialists now routinely check for and treat ongoing infections, nutritional deficiencies and low thyroxine levels17.
In the UK, researchers have found that lifestyle advice e.g. about expenditure of energy, diet etc. plus stress management and counselling, can significantly reduce disability and distress18.
As far as exercise is concerned, those who do not engage in 'excessive rest' or who tend to operate at their own activity ceilings should learn to pace themselves through the day18. However, for people whose fatigue appears to be maintained by unhelpful beliefs and behaviours, cognitive-behaviour therapy (CBT) plus graded activity is the treatment of choice19.
In my opinion, the question to be answered is not so much whether patients should exercise but how much and when. NB. 'Graded' means that patients cannot reduce or stop activity when they feel ill, while gentle exercise and pacing are more flexible.
Looking back over the literature on CFS, this decade was dominated by psychobabble and some very biased reporting in the UK medical press. However, science always rights itself and things are improving. What people need now, apart from more editorial balance in the medical journals, are two things. Firstly, we need better criteria to separate the different fatigue syndromes. Without them, researchers will continue to report inconsistent and confusing findings (see studies of cortisol levels, prevalence of depression, abnormalities of concentration and memory etc.). Secondly, doctors must begin to trust people with CFS. The message of the past ten years, seems to have been 'don't believe what your patients say.' In addition, the doctors and scientists who challenged this irrational attitude were isolated and insulted. It's a highly unscientific approach which not only caused a great deal of unnecessary hostility, but also wasted valuable time. Good science demands an open-mind, and that means listening to and respecting those with a different view20.
Dr. Ellen Goudsmit. Chartered Health Psychologist.
1. Fukuda et al. Annals of Internal Medicine, 1994, 121, 953-959. (Current CDC criteria with references to older versions) For a definition of ME see Dowsett and Welsby, Postgraduate Medical Journal, 1990, 526-530.
According to Dr. Melvin Ramsay, who wrote the most detailed descriptions of the illness, the typical symptoms of ME can be categorised in terms of three components: fatiguability, cerebral dysfunction and circulatory impairment. Muscle fatiguability is a dominant feature of the illness. It comes on after comparatively little physical effort and a period of 24 hours to five days may elapse before full muscle power is restored. Particularly affected are the weight bearing muscles in the leg, but Ramsay added that weaknesses could also occur elsewhere. Thus fatigue in the sphincter muscle might result in increased frequency of urination, and weakness of the masseter muscle could lead to dribbling of saliva from the mouth. Delayed recovery of muscle function has been documented (using objective tests) in people with a ME-like illness (Wood et al, in press) but not, to my knowledge, in studies on general CFS.
The second component, cerebral dysfunction, is manifested by symptoms such as impaired memory and concentration, difficulties completing sentences and finding the right word, a reduced tolerance of loud noises, 'brain fatigue' and emotional lability. The third component could explain the facial pallor which is visible before a patient reports feeling ill, and having cold extremities, even when it's warm.
Other typical symptoms include blurred vision, giddiness, general muscle pains and twitchings, abnormally low temperatures and 'feeling awful'. Ramsay also noted the recurrence of sore throats, feeling faint (cf. recent research on blood volume), and the increasing sensitivity to foods and drugs. Furthermore, he described the typical fluctuations in the severity of the symptoms, he advocated pacing and was open-minded about supplements (Pulse, 1983, Jan. 15th, 48).
ME frequently follows infections, particularly during the months from May to November. The onset tends to be acute and sometimes biphasic, i.e. patients report an initial improvement, followed by a worsening. However, gradual onset cases are acknowledged.
The 1994 CDC criteria for CFS require the presence of profound, unexplained fatigue lasting six months or more, plus four symptoms out of a list of eight. These include impaired concentration or memory, post-exertional malaise, new headaches, unrefreshing sleep, muscle and joint pain, sore throat and tender glands. In other words, the focus is on fatigue rather than fatiguability, and one can qualify for a diagnosis of CFS without evidence of cerebral dysfunction.
As far as PVFS is concerned, some researchers believe it is identical to ME while others maintain that there are notable differences. In America, some patients prefer the term chronic fatigue and immune dysfunction syndrome (CFIDS). However, it's unclear how this differs from CFS and this name is rarely used in the medical press.
Articles discussing the heterogeneity of CFS include Jason et al. American Psychologist, 1997, 52, 9, 973-983. Laymen can find more information on ME and CFS in Dr. Anne Macintyre's new book ME (Chronic Fatigue Syndrome - A Practical Guide) (Thorsons, 1998).
2. Ho-Yen and McNamara. British Journal of General Practice, 1991, 41, 324-326. See also Wessely et al. American Journal of Public Health, 1997, 87, 9, 1449-1455. Note the similar estimates using the Oxford and CDC 1994 criteria for CFS.
3. Even a straightforward separation of acute and gradual onset cases has proved illuminating. For instance, acute onset cases have slightly different immune system abnormalities than those with a gradual onset and they are less often associated with psychiatric disorders and stress. Mawle et al. Journal of Infectious Diseases, 1997, 175, 1, 136-141 and Reyes et al. Journal of Chronic Fatigue Syndrome, 1996, 2, 4, 17-33. See also DeLuca et al, Journal of Psychiatric Research, 1997, 31, 1, 83-90 or Christodoulou et.al. In Yehuda, S and Mostofsky, DI (eds.) Chronic Fatigue Syndrome. NY: Plenum Press. 1997.
For a comparison of ME-like conditions and broadly-defined groups, compare Lerner et al with Surawy et al (details under notes 8 and 15).
4. ICD-10 is compiled by the World Health Organisation. It is acknowledged as the main classification system of disorders in the world. However, psychiatric illnesses tend to be diagnosed according to DSM-IV, a system compiled by the American Psychiatric Association but also used in the UK.
5. Costa et al. Quarterly Journal of Medicine, 1995, 88, 767-773, recently replicated using PET scans by Tirelli et al. American Journal of Medicine, 1998, 105, 3A 54s-58s. See also Costa and Richardson, Journal of Chronic Fatigue Syndrome, 1998, 4, 3, 23-38, and Schwartz et al. American Journal of Roentgenology, 1994, 162, 4, 943-951.
6. McGarry et al. Annals of Internal Medicine, 1994, 120, 11, 972-973.
7. Lane et al. Journal of Neurology, Neurosurgery and Psychiatry, 1998, 64, 362-267. See also Behan et al. Acta Neuropathologica, 1991, 83, 61-65 and Kuratsune et al. International Journal of Molecular Medicine, 1998, 2, 1, 51-56.
8. Lerner et al. Infectious Diseases in Clinical Practice, 1997, 6, 110-117. This study describes patients suffering from CMV who were helped by taking ganciclovir.
9. Hassan et al. Clinical Immunology and Immunopathology, 1998, 87, 60-67. See also Bennett et al, Journal of Clinical Immunology, 1997, 17, 3, 253-261 and Landay et al, Lancet, 1991, 338, 707-712.
10. See Landay et al and Hassan et al, above.
11. Martin and Anderson. Pathobiology, 1997, 65, 51-56 and Martin, ibid, 1997, 65, 57-60.
12. Conference report, Sydney 1998.
13. Bowles et al. Journal of Medicine, 1993, 24, 145-160.
14. Vojdani et al. Journal of Internal Medicine, 1997, 242, 6, 465-478.
15. Surawy et al. Behavior, Research and Therapy, 1995, 33, 535-544. See also Hickie et al. Psychological Medicine, 1995, 25, 925-935. Most of the research on broadly defined groups has failed to find the type of abnormalities reported in more strictly defined populations (e.g. the work by the Nijmegen team, the research by the CFS unit at King's etc.).
16. Hock. Journal of Chronic Fatigue Syndrome, 1997, 3, 3, 117-127 (re vitamin D). See also Borok, ibid., 1998, 4, 3, 39-57 (re food sensitivities) and Regland et al, Scandinavian Journal of Rheumatology, 1997, 26, 301-307 (B12).
17. Teitelbaum and Bird. Journal of Musculoskeletal Pain, 1995, 3, 4, 91-110. A drug of the future is Ampligen. However, it is probably not suitable for everyone with CFS.
18. Goudsmit. The Psychological Aspects and Management of CFS. PhD Thesis. 1996. Available from the British Thesis Service in various forms (phone 01937 546229).
19. Wessely et al. Chronic Fatigue and its Syndromes. Oxford University Press. 1998. This includes a detailed description of the personality, beliefs, and behaviour of patients who respond to CBT and graded exercise. However, it does not describe ME. See also Jason et al1 for critical comments, and note that graded exercise has not yet been tested in people with pure ME or PVFS.
20. See Wessely et al, note 19 and Surawy et al, note 15, for illustrations of this sceptical approach. Also recall that the Working Party who wrote the Royal Colleges Report did not include a single ME specialist or expert who disagreed with the CBT model.
For years, I have advocated pacing as a strategy for coping with the illness. However, as a result of experience AND the latest research, I can now refine this advice. So in addition to pacing, Id like to introduce the concept of switching. Switching means changing activities to avoid tiring specific muscles. For instance, if youve been reading for a while, stop before your eye muscles get tired and do something which involves a different muscle group, e.g. walking, washing clothes, eating, talking. Do that for a while (stop before you reach your limit), then switch again (you can even go back to reading).
The research behind pace and switch is the work by Paul et al (1999) - They found that our muscles lose strength in the same way as healthy people during exercise but that unlike everyone else, we continue to lose strength afterwards. A Consultant (who has been studying ME since 1955) wondered if stopping an activity before the tiredness set in might keep the additional loss of muscle strength to a minimum. He began switching, and it worked for him.
I know that its not easy to stop activities which you havent finished but on the other hand, if you can extend your energy levels this way, why not give it a try?
The same rule applies to mental exertion (i.e. switch before you start feeling tired). Also, remember to balance physical and mental activities with rest (and that doesnt mean watching TV). If youre in a relapse, you may have to be strict i.e. physical activity - rest - mental activity - rest etc. However, as you improve, you should be able to do more and rest less without paying for it. See what and how much you can manage in a day using this new method. It takes some self-discipline but what have you got to lose?
Ellen Goudsmit (Dr.)
Chartered Health Psychologist
Copyright Dr. EM. Goudsmit September
Chartered Health Psychologist/Archivist, London.
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