MEDICAL UPDATE Spring 2000

Moss, RB et al.  TNF-α and chronic fatigue syndrome.  Journal of Clinical Immunology, 1999, 19, 5, 314-316.

These researchers wondered if certain cytokines play a role in CFS. Cytokines form part of the body's response to infection and cancer and include interleukins, interferons and tumour necrosis factors (TNF). The cytokine studied here was TNF-α.  It's involved in inflammation and healing but side effects include fatigue and pain.

The study tested the blood of 240 people with CFS and 240 healthy controls. The results revealed a highly significant increase in the levels of TNF-α in the patient group as a whole, though only 32% had levels above 50 pg/ml (compared with 7% of the non-CFS controls).

There have also been a number of other studies showing raised levels of cytokines in CFS (e.g. Cannon et al, Journal of Clinical Immunology, 1999, 19, 6, 414-421.) However, most of the evidence suggests that cytokine dysregulation is probably a result, rather than a major cause of the illness.

Lange G et al. Brain MRI abnormalities exist in a subset of patients with chronic fatigue syndrome. Journal of the Neurological Sciences, 1999, 171, 1, 3-7.

The researchers studied the MRI scans of three groups: 21 patients with CFS (modified CDC criteria' 94) but no psychiatric disorder (CFS-No Psych); 18 people with CFS plus a psychiatric disorder (CFS-Psych), and 19 sedentary healthy controls (HC).

MRI scans show the structure of the brain, not how it functions.

The CFS-No Psych group had a significantly larger number of brain abnormalities than the CFS-Psych and HC groups, particularly in the white matter and more specifically, in the frontal lobes.  These findings could explain the "more severe cognitive impairment previously reported in this subset of CFS patients". No differences were found when both the CFS groups were combined and compared to the controls.

The results are consistent with earlier reports of structural abnormalities in some patients with CFS (e.g. Buchwald et al). They also support the view that further studies should focus on subgroups, rather than mixed samples.

Wood, B and Wessely, S. Personality and social attitudes in chronic fatigue syndrome.  Journal of Psychosomatic Research, 1999, 47, 4, 385-397.

This study on 101 patients with CFS (Oxford and CDC criteria '94) and 45 people with rheumatoid arthritis (RA) found no difference on measures such as perfectionism, attitudes to mental illness, 'harm avoidance' and depression.

According to the researchers, the findings fail to support "media and self-help stereotypes" of the "high-achieving, over-dedicated sufferer with high personal standards" and hostility towards all things psychiatric. They also note that depressive disorders in their CFS clinic "have been decreasing over time", which they attribute to better recognition and treatment by GPs (rather than improved diagnosis of CFS by researchers.)

Aside from the diagnostic criteria (which are too broad), it's hard to fault the study itself. However, I'm not so sure about the discussion of the results. For example, my archive indicates that the origin of the perfectionist stereotype was not the media, nor the self-help literature, but the opinions of a small group of sceptical researchers and clinicians, one article by a social anthropologist with no previous experience of CFS and a few anecdotal, and often ambiguous reports. The sceptical medical professionals were also responsible for insinuations about these patients sharing a particularly hostile attitude towards psychiatry.

Christodoulou, C et al.  Examination of Cloninger's basic dimensions of personality in fatiguing illness: chronic fatigue syndrome and multiple sclerosis.  Journal of Psychosomatic Research, 1999, 47, 6, 597-607.

In this study on personality, the researchers compared 38 patients with CFS (modified CDC criteria '94), 40 patients with multiple sclerosis (MS) and 40 healthy controls.

There were a number of similarities between the CFS and MS groups, suggesting that "different forms of illness can alter personality in similar ways."  At the same time, there was no evidence that the CFS patients possessed "an unusual level of negativity that would have predisposed them to develop their illness, any more so than MS patients".

Christodoulou, C et al. Acquisition, storage and retrieval of verbal material in chronic fatigue subjects with and without psychiatric co morbidity. Archives of Clinical Neuropsychology, 1999, 14, 8, 652.

This abstract summarises the findings of a study involving 51 patients with CFS, of whom 22 had a psychiatric illness and 29 did not. They were compared with two control groups: 30 healthy persons and 19 people with rheumatoid arthritis. Verbal memory was assessed using a word list learning task.

The results indicate that the two CFS groups required more trials to learn the word list than the healthy controls.  During recall, the CFS patients without psychiatric disorders performed more poorly than the healthy controls. There were no significant group differences for recognition.

The results imply that verbal memory impairment in CFS is caused by problems in acquisition.  The patients without psychiatric disorders also exhibited deficient retrieval from long-term storage (memory). In other words, the problems with memory are specific, not global, and again, it's clearly worth studying subgroups.

Best of the rest

Ware, NC. Toward a model of social course in chronic illness: The example of chronic fatigue syndrome. Culture, Medicine and Psychiatry, 1999, 23, 3, 303-331.

A new article by Harvard anthropologist Dr. Norma Ware discusses the social effects of having CFS.  It's an excellent paper, challenging the stereotype of the not-very-sensible, highly phobic patient so prevalent in the UK.

Ziem, GE. Profile of patients with chemical injury and sensitivity, part II. International Journal of Toxicology, 1999, 18, 6, 401-409.

Interesting article on multiple chemical sensitivity and its relationship with CFS. It lists some of the metabolic, endocrinological, immunological and gastrointestinal abnormalities that may be involved in the aetiology of MCS.

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