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Chronic fatigue syndrome: fatigue of unknown origin

Fatigue is a symptom accompanying many conditions and diseases such as infections, inflammation, injury and operations, reconvalescence, overtraining [1], depression, the aftermath of panic, cytokine therapy (interleukin 2, interferona), states of fever, heat or cold stress, severe mental effort and a great number of specific diseases. But the cause of fatigue is not always apparent to the patient or his or her doctor, and this problem is so important that it has received status as a health care problem in its own right: chronic fatigue syndrome (CFS) [2,3]. In this issue of the journal (p. 000) Professor Dickinson presents a new approach towards solving the enigma of CFS. Medical science has tried to consider it either as a disease or as a behavioural, psychological or psychiatric problem. As to the first, no definite proof of the presence of a pathological defect has yet been found, but Professor Dickinson suggests that this view must be changed to take account of small multiple patchily distributed neuronal lesions affecting the reticular activating system (RAS) of the upper brain stem. One study has shown reduced regional blood flow in the brain stem, and this finding is still under discussion [4]. Comparison with fatigue in poliomyelitis and multiple sclerosis (MS) suggests that histological damage to the RAS might be the cause of chronic fatigue in CFS if, indeed, this is also the cause of fatigue in polio and MS. Data pointing to the association between CFS and lesions viewed by magnetic resonance imaging (MRI) are variable. Although statistically significant, they do not prove that these punctate lesions are the cause of the fatigue, which is a basic problem of the epidemiological method. Epidemiological evidence leads to suspicions or hints and may help to formulate testable hypotheses. How is fatigue explained in the absence of lesions in the RAS? Is it conceivable that punctate lesions would cause a soft sign such as fatigue without a hard neurological symptom such as an irreversible decrease in consciousness? Some unsuspected cases of MS have been detected. The important question about punctate lesions found by MRI is what their significance actually is. Often MRIs reveal small white matter lesions that cannot be linked to a specific pathological function—should all such patients be diagnosed as subclinical cases of MS or viral encephalitis? These would be specific diagnoses of known diseases instead of the riddle that is CFS. Is another approach possible instead of the old dichotomy of pathology vs. psychology, which is still apparent in the literature cited by Professor Dickinson? It is time for clinical medicine to catch up with the enormous advances made in basic psychobiological science. We have left behind the old Cartesian body–mind dualism simply because it does not exist. Every psychological phenomenon has a physiological substrate. The substrate is not the cause of psychology, nor is the latter the cause of physiology. Like the chicken and the egg, they have emerged together and are inseparable. What we observe is merely a result of the tools we use. Chronic fatigue can be explained without the need for a new hypothesis. It mainly requires a reappraisal of the significance of structural change as a substrate of pathology and psychology and that the nineteenth-century disease concept still commonly in use be discarded. The consistency of the disease concept of CFS could be critically discussed. The solution to our problem is likely to be found at this level. Is fatigue, when named as such by patients, a homogeneous symptom or can it have different connotations? In my experience the latter is usually the case. Is CFS a homogeneous ‘syndrome’? Can it be discriminated unequivocally from other syndromes, e.g. fibromyalgia or depression? Has it been sufficiently validated [5]? Does a sign or symptom make a syndrome even if this seems to be the core? We do not take fever to be a ‘syndrome’. When we speak of fever of unknown origin (FUO), we consider it as a symptom of a disease to be diagnosed. Would it not be more sensible, then, to speak of ‘fatigue of unknown origin’? The nineteenth-century disease model typically had specific infectious diseases with characteristic symptoms as its guiding principle. The paradigm was ‘one cause— one disease’. By now, we know that there is no monocausality and that a single pathogenic agent does not always have the same phenomenological consequences. Neither is a seemingly uniform syndrome always caused European Journal of Clinical Investigation (1997)27, 268–269