|
Volume 1, number 1 |
ME
AND CFS
|
1st March 1998 |
Ten years after we noted that the term CFS covered a number of conditions, top virologist Dr. Stephen Straus has apparently come to the same conclusion. According to a fellow sceptic, this highly influential researcher recently described CFS as "a mixed bag of entities". And there's even better news from Britain! In a recent medical journal article by Professor Simon Wessely and Dr. Michael Sharpe, both authors acknowledged the need to study subgroups! That may not seem like a revolutionary statement to you, but believe me, it is!
What a great pity that these doctors didn't believe us back in 1988. Think of all the time and money they could have saved! Alas, they chose to go their own way, dismissing the ME specialists as naive and ignoring any evidence to the contrary. What's even sadder is that they isolated all those with a different view, not only refusing to invite them to conferences but also barring them from the main-stream medical journals (through their work as referees etc.).
The result of all this intolerance is that British doctors have read only one side of the story. Moreover, it has stifled debate and resulted in second-class research.
But now the controversy is over. Even that most conservative body of experts, the American Centers for Disease Control, is apparently rewriting its booklet for American doctors, to include news of the subgroups. What they will probably say is that:
1. CFS is not a single entity/illness/disorder and
2. some subgroups may be the result of ongoing disease.
Of course, British doctors need to know this too, but which medical journal will update them? My article on the subject has been rejected by every editor who's seen it. Admittedly, I'm not the world's most eloquent writer, but having been made aware of the recent developments, the editors could have commissioned someone else to cover this research. And so far, they haven't.
Personally speaking, I hope that Prof. Wessely will respond to the new developments with wisdom and grace, and that he will finally give the ME specialists the credit they deserve. In a way, we were all right, but just talking about different things. Secondly, I hope that he will join the Americans and look again at what we used to call ME. And lastly, I hope that I won't be writing in ten years time that he refused to listen, or that he was the last researcher to realise the significance of what we had observed.
This is a good time to put the past behind us. So let's forget the frustrations of the years gone by and focus on the future. To start with, here are some of the questions which I myself would like an answer to:
1. Do subgroups other than ME also show the close relationship between symptoms and exertion?
2. Are the fluctuations which characterise ME/PVFS also found in other fatigue syndromes?
3. Are summer bugs more likely to trigger fatigue syndromes than winter bugs (some researchers believe that they do).
4. What happens to the blood-brain barrier in people with fatigue syndromes?
A final thought. If there is any lesson to be learned from this episode in medical history, it must be that researchers and clinicians who don't listen or believe their patients will almost certainly mistakes. If you should come across anyone like that, here are some new findings to discuss with them.
Bennett, A et al. Elevation of bioactive transforming growth factor-b in serum from patients with chronic fatigue syndrome. Journal of Clinical Immunology, 1997, 17, 2, 160-166.
The level of bioactive transforming growth factor-b (TGF-b) was measured in blood samples from 93 patients with CFS (CDC criteria '88 plus post-exertional malaise), 80 healthy controls, 46 patients with major depression, 50 patients with systemic lupus erythematosis and 57 patients with multiple sclerosis.
Patients with CFS were found to have significantly elevated levels of bioactive TGF-b compared with the other groups.
We don't know why the levels of this cytokine were raised. They could reflect the body's attempt to suppress an inflammatory response, but they may also be part of an attempt to protect brain cells from some other kind of injury (they're also raised in Alzheimer's disease). Either way, this finding replicates earlier work and is therefore fairly robust. Moreover, given the fact that it was not found in depressed patients nor in people with active MS, it's hard to attribute the abnormality to alterations in mood or lack of fitness (for the latter view, see a recent editorial by White, J. Psychiatric Research 1997, 43, 4, p. 347).
Incidentally, the researchers used an additional criterium to select the patients with CFS. It is likely that the presence of post-exertional malaise will have increased the proportion of patients with the fatigue syndrome formerly known as ME.
Vojdani, A et al. Elevated apoptotic cell population in patients with chronic fatigue syndrome: the pivotal role of protein kinase RNA. Journal of Internal Medicine, 1997, 242, 465-478.
Blood samples taken from 29 people with CFS and 15 healthy individuals showed that the former had an increase in programmed cell death (apoptosis), and raised levels of protein kinase RNA (PKR) compared with the controls. In addition, more of the former had raised levels of the cytokine interferon-a than the latter.
According to the researchers, these results could be the result of a disregulated immune system or the presence of a chronic viral infection. They are currently examining whether this can be reversed using certain drugs.
Incidentally, PKR has tumour suppressor properties. I mention this because I think that women with CFS have a much lower prevalence of breast cancer compared with the general population. Could that be due to the raised levels of PKR?
Lindal E et al. Anxiety disorders: A result of long-term chronic fatigue - the psychiatric characteristics of the sufferers of Iceland disease. Acta Neurologica Scandinavica, 1997, 96, 3, 158-162.
The aim of this study was to assess the likelihood of developing psychiatric disorder following the outbreak of Akureyri disease (i.e. epidemic ME).
The researchers investigated 55 well documented cases of Akureyri disease who were still experiencing symptoms. All participants were interviewed and the results were compared to those of 421 members of the general population.
Of the 55 subjects included in this analysis, 53 were women. The mean age of the participants was 67.7 years. The following disorders were found more commonly among the patients than the controls: agoraphobia with panic attacks 12.7%; agoraphobia without panic attacks 21.8%; social phobia 14.5%; simple phobia 18.1%; schizophrenia 3.6%; and alcohol dependence 5.3%. The rate of recurrent major depression was also higher than in the controls (5.4%) but the difference did not reach significance.
When the patients were compared with 10 people suffering from systemic lupus erythematosus (SLE), the only significant difference was in the prevalence of lifetime generalised anxiety.
The researchers conclude that prolonged chronic fatigue most commonly results in anxiety disorders, particularly those relating to social conspicuousness. In other words, patients may become afraid of not being able to manage a whole social encounter etc. This is also found in people with SLE. "Following the infection, the more serious psychiatric disorders do not seem to play a major role in the long run."
This is an interesting report. While CFS appears to be associated with increased rates of depression, this study of ME suggests a closer link with anxiety. Didn't we tell you that studying subgroups would be illuminating?
De Lorenzo, F et al. Pathogenesis and management of delayed orthostatic hypotension in patients with chronic fatigue syndrome. Clinical Autonomic Research, 1997, 7, 4, 185-190.
These researchers used the upright table test to determine the presence of orthostatic hypotension in 78 patients with CFS (CDC criteria '94). The results were compared with those of 38 healthy controls. Patients found to have orthostatic hypotension (their blood pressure dropped, in some the heart rate increased and they felt faint) were offered therapy with sodium chloride for 8 weeks. They were then assessed again.
An abnormal response to the upright tilt test was observed in 28% of the patients with CFS. After sodium chloride therapy, 10 of the 22 developed orthostatic hypotension once more, but 11 did not. One did not complete the test.
In this mixed population, about a third formed a subgroup and half of these responded quickly to an increase in salt intake.
If you're interested in postural hypotension and related disorders, you suffer from palpitations, and you feel dizzy and faint on standing up, why not discuss this with your GP. (See also Grubb et al. Pace-pacing and Clinical Electrophysiology, 1997, 20, 9, 2205).
Incidentally, several researchers studying these symptoms believe that the cause may be reduced blood volume (cf. Yataco et al. Clinical Autonomic Research, 1997, 7, 293-297). Watch this space for further developments!
Bazelmans, E et al. The chronic fatigue syndrome and hyperventilation. Journal of Psychosomatic Research, 1997, 43, 371-377.
This article reports three studies on patients with CFS (Oxford criteria). Study 1 showed that only 19% of the CFS patients and none of the controls met strict criteria for hyperventilation.
The other studies indicated that although significantly more CFS patients hyperventilated compared with controls, the CFS patients with hyperventilation did not differ from those without.
According to the researchers, hyperventilation does not play a substantial role in causing or perpetuating the condition.
Journal of Psychiatric Research, 1997, 31, 1. Selected presentations from the American Association for Chronic Fatigue Syndrome Conference, Florida, 7-9 October 1994.
Jason, LA et al. Politics, science, and the emergence of a new disease. The case of chronic fatigue syndrome. American Psychologist, 1997, 52, 9, 973-983.
This article examines the controversy surrounding CFS. The authors note the differences between the narrow and broader criteria currently in use and suggest that the latter may have resulted in more heterogeneous (mixed) groups. They also point out that tests used to assess psychiatric disorders can lead to inaccurate results. For instance, one study compared two different measures: the DIS and SCID. The DIS diagnosed 50% of the patients as having a current psychiatric illness whereas the SCID led to a similar diagnosis in only 22%.
The authors add that the bias of some researchers towards a psychiatric explanation may have filtered down to the media which have consequently portrayed CFS in simplistic and stereotypical ways.
The article goes on to list several differences between CFS and depression (e.g. the former has a higher incidence of severe fatigue, nausea, post-exertional malaise, flu-like symptoms and intolerance to alcohol). They state that the depression which accompanies a long illness should be regarded as demoralisation rather than as a discrete psychiatric condition.
With regard to treatment, the authors note the difficulties in interpreting the data from trials of cognitive-behaviour therapy (CBT). For instance, studies to date have varied in terms of the severity of symptoms, the percentage of patients with psychiatric illness etc. They agree with Friedberg and Krupp that CBT is appropriate if activity is avoided due to depressed mood and an unrealistic fear of relapses. However, if this does not apply, they recommend a tailor-made rehabilitation programme to meet the needs of the individual patient, their symptoms and actual activity levels.
Finally, the authors suggest that the current criteria require clarification and that the inclusion of different illnesses under the label of CFS makes it difficult to interpret the data (see the last Update).
This important paper, published in an influential journal, challenges the validity of the best-known psycho-social theory of CFS.
Ray, C et al. Coping and other predictors of outcome in chronic fatigue syndrome: A 1-year follow-up. Journal of Psychosomatic Research, 1997, 43, 4, 405-415.
In this prospective study, 137 patients with CFS were followed-up for a year. All patients fulfilled the Oxford criteria with the additional requirement of exercise-induced fatigue precipitated by relatively trivial exertion (i.e. a criterium for PVFS/ME). After investigating alternative explanations of their symptoms, the patients were recommended a regime of rest balanced with modest exercise, together with a meditation technique to help reduce psychological stress. Patients with apparent depressive illness were given low-dose antidepressants.
At follow-up, 64.4% reported improvement and 14.8% reported a worsening of symptoms. Fatigue and disability at this time were related to the duration of the illness, cognitive difficulty and somatic symptoms. There was no influence of anxiety, depression or illness attributions.
The commonly used strategy of 'accommodation to the illness', where patients plan their activities to avoid overexertion and stress, was related to a poor outcome but only when the patient felt no control over their recovery. The researchers suggest that interventions that discourage avoidance of activity and/or enhance perceived control could benefit the course of the illness.
This follow-up study challenges the CBT explanation which predicts that believing in a physical cause leads to a reduction in activities and increased fatigue. Moreover, the conventional coping strategy (rest and avoiding overexertion) was not linked with poor outcomes overall (over 60% improved). Finally, a person's belief that they can do something to recover is very important. This can be achieved in a number of ways, not just through CBT.
Lapp, C. American Journal of Medicine, 1997, 103, 83-84.
In this letter, Lapp reports a trial involving 31 consecutive CFS patients who were asked to record their symptoms on a simple scale starting three weeks before and finishing 12 days after exercise testing (cycling).
The results showed that 74% of patients experienced worsening fatigue and 26% stayed the same. None improved. The average relapse lasted 8.82 days although 22% were still in relapse when the study ended. Aside from fatigue, there were increases in lymph pain, sore throat, depression, abdominal pain, sleep quality as well as joint and muscle pain. These findings contrast with those from previous studies which found no or little worsening of symptoms following exercise (cf. research by Wessely et al, Sharpe et al).
According to Lapp, patients can do mild to moderate exercise or work without relapse providing they have frequent rest periods. He advises his own patients to follow short periods of activity with rest. This work-rest cycle may be repeated several times daily in order to maintain strength, flexibility, and conditioning.
Lapp's previous descriptions of patients suggest that he sees many people with PVFS/ME. The presence of significant post-exertional fatigue may be one difference between ME and more common fatigue syndromes such as burn-out and TATT (tired-all-the-time).
Hock, AD. Journal of Chronic Fatigue Syndrome, 1997, 3, 3, 117-127.
This study suggests that some patients with unexplained chronic fatigue may be lacking vitamin D. This is easily remedied with a prescription supplement.
Packer, TL et al. The Occupational Therapy Journal of Research, 1997, 17, 3, 186-199.
According to these researchers CFS patients spend less than 17% of their day time resting. This supports objective measures (Vercoulen 1997) indicating that people with CFS are no more inactive than people with mild MS. In other words, the notion of 'excessive rest' and 'total inactivity' in all patients with CFS is a myth!
If you wish to read any of the papers above, please contact your local library.
1. ME is regarded as an organic disease by the World Health Organisation.No, life isn't that simple. Although ME was listed under diseases of the nervous system in 1982, 'fatigue syndrome' is classified under 'neurotic' disorders. If the WHO do not obtain sufficient evidence that ME is a separate subgroup, I suspect that they will delete it from ICD-11 (due 2002) and classify all fatigue syndromes under mental and behavioural disorders.
2. Exercise can cause permanent damage.
This is a generalisation which is difficult to substantiate. Overexertion can trigger a relapse, but I haven't seen any evidence that gentle exercise causes permanent damage.
1. CFIDS stands for chronic fatigue and immune deficiency syndrome.2. CFIDS and ME are 'belief systems'.
3. Clare Francis founded Action on ME.
4. Colonic lavage is now a common treatment for ME in the UK.
5. Electrical treatments and diagnosis flourish for ME.
Well, those reading the article CFS: a 20th century illness by Simon Wessely (Scand. J. Work Environ. Health 1997, 23 suppl. 3, 17-34), will believe all the above are true. On the other hand, those of you who regularly struggle through our Medical Updates will know that the D in CFIDS stands for dysfunction, that ME is the old name for some patients with CFS, that Clare Francis was president of Action for ME, and that statements 4 and 5 are major exaggerations. Of course, Prof. Wessely knows what is truthful and what is not ('cause he reads this Update too), so quite why he continues to portray ME patients as weird, wacky and seriously stupid is quite beyond me.
Combined, the following three reviews provide a much more accurate picture of CFS than the Royal Colleges Report.
Komaroff, A. Journal of the American Medical Association, 1997, 278, 14, 1179-1185.Plioplys, AV et al. Hospital Practice, 1997, 32, 6, 147-166.
Shepherd, C. British Journal of Social Work, 1997, 27, 755-760.
Copies can be obtained though your local library.
Copyright EM. Goudsmit 1998.
©
All rights reserved. This article may not be reproduced without
permission from the author. See the full
copyright
notice.
Be sure to see the many other valuable articles at our Main M.E. Home Page
