MEDICAL UPDATE Spring 1999

Paul, L et al. Demonstration of delayed recovery from fatiguing exercise in chronic fatigue syndrome. European Journal of Neurology, 1999, 6, 63-69.

One of the main differences between ME and most cases of CFS is the phenomenon of prolonged muscle fatigue after minimal exertion. However, the research on muscle function during and after exercise has been far from illuminating. Some studies (on patients with CFS) have found an abnormality during exertion but most have not. Moreover, none have detected an obvious problem during the recovery phase. On the basis of this research, psychiatrists claimed that the vast majority of fatigued patients don't have anything wrong with their muscles and that exercise when tired was therefore safe. However, it is now generally accepted that CFS covers a number of disorders, so what is safe for one fatigue syndrome may not be safe for another.

The following study illustrates this point. Researchers from Glasgow recently assessed muscle strength during a series of strenuous tests and up to 24 hours afterwards. The subjects included 10 patients with 'CFS' (diagnosed using criteria consistent with ME) and 10 sedentary controls.

The results revealed that the patients with CFS/ME were weaker at the beginning of the tests compared to the controls, although the decline in muscle power during the exercise was the same. The most interesting finding, however, was that the CFS/ME patients showed a decline in muscle strength during the recovery phase when the muscles of the controls were getting stronger. The difference between the groups was particularly marked at 24 hour post-exercise.

There are a number of explanations for the abnormalities but given the results were compared to sedentary controls, deconditioning isn't one of them. While we speculate, it may be wise to think again about the advice to exercise beyond fatigue, at least for people with ME/PVFS.

Scholey, A et al. A comparison of the cognitive deficits seen in myalgic encephalomyelitis to Alzheimer's Disease. Proceedings of the British Psychological Society, 1999, January, 12.

Another symptom which is characteristic of ME is impaired cognitive functioning (e.g. poor memory etc.). Early reports revealed major deficits but these were forgotten when the research found only subtle changes in CFS. The following study is noteworthy because it focused exclusively on people with ME (London criteria).

Tests were done on 20 patients and it was found that their performance was significantly inferior to that of healthy controls. Moreover, when the results were compared to those from 782 patients with Alzheimer's Disease (AD), the ME group fell between mild and moderate Alzheimer's patients on most tasks. "The extent as well as the range of the impairments ... confirms the severe nature of ME."

These findings deserve to be taken seriously because they were reported by one of Britain's leading experts in the field. The results not only support anecdotal reports from patients but they underline once again that generalisations about CFS may not apply to the various subgroups.

Conti, F et al. Decreased immunoreactive beta-endorphin in mononuclear leucocytes from patients with chronic fatigue syndrome. Clinical and Experimental Rheumatology, 1998, 16, 729-732.

Blood samples were taken from 16 patients with CFS (CDC criteria '94, only 11 with post-exertional malaise). It was found that concentrations of the opioid beta-endorphin were lower in the patients compared to the 10 healthy controls.

According to the researchers, this is more evidence of chronic immune activation in CFS.

Choppa PC et al. Multiplex PCR for the detection of Mycoplasma fermentans, M. hominis and M. penetrans in cell cultures and blood samples of patients with chronic fatigue syndrome. Molecular and Cellular Probes, 1998, 12, 5, 301-308.

Blood collected from 100 people with CFS (CDC criteria '94) revealed a relatively high incidence of mycoplasma (the smallest type of bacteria) compared to healthy people. Indeed, the mycoplasma infection rate was 52% in CFS patients and 15% in the controls. For those who like details, mycoplasma fermentans, M. hominis and M. penetrans were detected in 32, 9 and 6% of the CFS patients while they were detected in 8, 3 and 2% of the controls, respectively.

The role played by mycoplasma remains uncertain. On the one hand, earlier studies found M. fermentans in saliva samples from healthy controls, suggesting that it is a benign coloniser of the oral mucosa. On the other hand, it was the only infectious agent identified in biopsies and blood samples taken from previously healthy non-AIDS patients with severe chronic fatigue or a flu-like illness. These patients recovered following adequate antibiotic therapy. Mycoplasma have also been implicated in Gulf War Syndrome.

In short.

According to certain psychiatrists, people with CFS respond in a uniform way to "fatigue" and their attempts at coping (e.g. 'total rest') are largely irrational and unhelpful. This theory forms the basis for graded exercise and cognitive-behaviour therapy though there is actually very little evidence which supports it (see article on CBT, elsewhere).

The latest findings challenging the psychiatrists' explanation comes from researchers based at Harvard University. They reported that many patients cope relatively well in the circumstances and that there is little difference between CFS and other chronically ill patients (Saltzstein et al. General Hospital Psychiatry, 1998, 20, 5, 307-316). Moreover, they found no evidence for the view that CFS is an 'illness behaviour' resulting from a need to opt out of work or family obligations. Important factors influencing recovery were early diagnosis, a doctor's validation of the illness, and intensive medical follow-up.

Finally, CT scans on 8 patients with CFS who also had evidence of adrenal dysfunction found a 50% reduction in the size of the adrenal glands (Teh et al, Radiology, 1998, 209P, Suppl. 411-412). This shows that it is important to measure cortisol levels and to treat CFS seriously.

Copyright EM. Goudsmit 1999. ©
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