MEDICAL UPDATE November 1998

NEW RESEARCH

Here is my choice of the most interesting research published in the past few months:

Tirelli et al. Brain positron emission tomography (PET) in chronic fatigue syndrome: preliminary data. American Journal of Medicine, 1998, 105, 3A, 54s-58s.

These PET scans assessed the functioning of the brain by focusing on the metabolism of glucose. (PET is more precise than SPECT, especially if one wants to study areas like the brainstem).

The scans of 18 patients with CFS were compared to those from 6 people with depression and 6 healthy controls. The patients were found to have abnormalities in the brainstem which were not present in the other groups. There were also abnormalities in the right mediofrontal cortex while people with depression had abnormalities in the medial and upper frontal areas.

The brainstem abnormalities support the findings reported by Costa and his team several years ago. They tested ME patients using SPECT and found reduced blood flow in this area; something which has not been documented in any other disease. Similar results were also obtained by Richardson and Costa (J. of Chronic Fatigue Syndrome, 1998, 4, 3, 23-57).

According to Tirelli et al, the abnormality in the brainstem may be a diagnostic marker for CFS. However, the cost of the scans and the lack of scanners means that it is not likely to become a test which one can ask for in the UK.

Blackwood, SK et al. Effects of exercise on cognitive and motor function in chronic fatigue syndrome and depression. Journal of Neurology, Neurosurgery and Psychiatry, 1998, 65, 541-546.

This study compared the performance on memory and attention tasks of 10 patients with CFS, 10 people with depression and 10 healthy controls. The tests were completed before and after exercise.

Before the exercise, there were no significant differences between the groups. However, after the exercise, the CFS group showed greater impairments on attention tests than either the depressed patients or the healthy controls.

The problem with interpreting these findings is that the patients with CFS were selected using broad criteria. It is not clear, therefore, how many might have had ME/post-viral syndrome. However, an American study on a much more clearly defined group found similar deficits on cognitive tests. In this research, the impairments affected the speed of information processing, rather than attention (see LaManca et al, American Journal of Medicine, 1998, 105, 3A, 59s-65s). What we can conclude from this is that exercise clearly has an adverse effect on cognitive function in people with CFS. This supports anecdotal reports from patients and provides more evidence of the difference between CFS and depressive mood.

Levine, PH et al. Dysfunction of natural killer activity in a family with chronic fatigue syndrome. Clinical Immunology and Immunopathology, 1998, 88, 1, 96-104.

This is a report on a family in which 5 out of 6 siblings and 3 other family members suffered from CFS. Tests revealed that they had much lower natural killer (NK) cell activity than unaffected family members and healthy controls. Some of the unaffected family members also showed reduced values, suggesting that low NK activity may be the result of a genetic abnormality predisposing them to CFS. NK cells are a part of the immune system and involved in fighting infection and cancer.

MISCELLANEOUS

Harlow et al studied 150 women with CFS and found a higher incidence of gynaecological conditions like missed periods (amenorrhoea), sporadic bleeding between periods, irregular cycles, hirsutism and ovarian cysts compared to women without CFS. In contrast, they reported fewer pre-menstrual symptoms prior to their illness, showing that women with CFS are not simply somatizers with a tendency to overreport all symptoms and illnesses (American Journal of Medicine, 1998, 105, 3A, 94s-99s).

In England, Castell et al measured levels of free tryptophan (the 'raw material' from which serotonin is made) and found higher than expected levels in patients with CFS compared to healthy controls. This and other findings suggest that people with CFS may have increased levels of serotonin, which could lead to fatigue and explain the often poor response to those anti-depressants which work by raising serotonin levels (Journal of Physiology, 1998, 509p, 206). Serotonin is one of the chemicals (neurotransmitters) implicated in depression and sleep disorders.

Finally, I was impressed by two studies from Kuratsune et al. In the first, they found reduced levels of acylcarnitine in the blood of Swedish patients with CFS. This replicates earlier research on people from Japan. Acylcarnitine deficiency was also found in people with chronic hepatitis C, but not in other patient groups. Acylcarnitine may be related to cytokine production and it is thought to have antioxidant effects. (International Journal of Molecular Medicine, 1998, 2, 1, 51-56).

In the other study, this team found low levels of dehydroepiandrosterone sulfate (DHEA-S) compared with normal controls. Serum DHEA-S is a hormone which is secreted from the adrenal glands, and may be related to memory, stress, anxiety, sleep and depression. Therefore, the deficiency of DHEA-S might influence the neuropsychiatric symptoms in patients with CFS. (International Journal of Molecular Medicine, 1998, 1, 1, 143-146).

If you would like to see any of the papers above, please contact your local library.  

Copyright EM. Goudsmit 1998. ©
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