polio – American ME and CFS Society

Abstract:

The chronic fatigue syndrome (CFS) has been intensively studied over the last 40 years, but no conclusions have yet been agreed as to its cause. Most cases nowadays are sporadic. In the established chronic condition there are no consistently abnormal physical signs or abnormalities on laboratory investigation.

Many physicians remain convinced that the symptoms are psychological rather than physical in origin. This view is reinforced by the emotional way in which many patients present themselves. The overlap of symptoms between CFS and depression remains a source of confusion and difficulty. But even if all CFS patients were rediagnosed as depressives, this would not negate the possibility of an underlying organic cause for the condition, in view of the growing evidence that depression itself has a physical cause and responds best to physical treatments.

There is some evidence both for active viral infection and for an immunological disorder in the CFS. Many observations suggest that the syndrome could derive from residual damage to the reticular activating system (RAS) of the upper brain stem and/or to its cortical projections. Such damage could be produced by a previous viral infection, leaving functional defects unaccompanied by any gross histological changes.

In animal experiments activation of the RAS can change sleep state and activate or stimulate cortical functions. RAS lesions can produce somnolence and apathy. Studies by modern imaging techniques have not been entirely consistent, but many magnetic resonance imaging (MRI) studies already suggest that small discrete patchy brain stem and subcortical lesions can often be seen in CFS.

Regional blood flow studies by single photon-emission computerized tomography (SPECT) have been more consistent. They have revealed blood flow reductions in many regions, especially in the hind brain. Similar lesions have been reported after poliomyelitis and in multiple sclerosis–in both of which conditions chronic fatigue is characteristically present. In the well-known post-polio fatigue syndrome, lesions predominate in the RAS of the brain stem. If similar underlying lesions in the RAS can eventually be identified in CFS, the therapeutic target for CFS would be better defined than it is at present. A number of logical approaches to treatment can already be envisaged.

Comment in:

Chronic fatigue syndrome. [Eur J Clin Invest. 1997]

Source: Dickinson CJ. Chronic fatigue syndrome–aetiological aspects. Eur J Clin Invest. 1997 Apr;27(4):257-67. http://www.ncbi.nlm.nih.gov/pubmed/9134372

Dr E.G. Dowsett is Honorary Consultant Microbiologist, Basildon and Thurrock Health Authority and is the President of the Myalgic Encephalomyelitis Society.

DR P.D. WELSBY: I, and indeed many general physicians, are often asked to see patients whose main complaint is ‘tiredness all the time (TATT)’. From my previous experience also of general practice it seems that there is a wide continuous spectrum of debility ranging from a few days or weeks, but sometimes, distressingly, lasting for years. Such illnesses may or may not follow symptoms of an infection. Does the Myalgic Encephalomyelitis (ME) Society differentiate between post-viral debility, postinfectious (often an undefined infection) fatigue syndrome, chronic fatigue syndrome and ME? If so, how, and should it make any difference to medical management?

DR E.G. DOWSETT: One of the most striking features of ME is that the patient is not tired all the time! Extreme and sudden variability of energy levels both within and between episodes of illness differentiate this syndrome from other diseases associated with fatigue. One can only deplore the current fashion in the United States as well as the United Kingdom to redefine and rename a disability which has been clearly described in the literature for at least 100 years.’ There is nothing to be said in favour of the American acronym CFIDS (chronic fatigue immune deficiency syndrome) with its connotation of a primary immune dysfunction. The term ‘chronic fatigue syndrome’ recently adopted in this country also is nonspecific and non-descriptive because most of the definition is based on a vast number of exclusions (some of which, for example, endocrine disturbance, are actually found in ME). ‘Post-viral fatigue syndrome’, another British name, describes one essential feature (the association of the illness with viral infection) but gives the impression that the infection was antecedent rather than, as we now know, persistent. I prefer to use the more specific term ‘myalgic encephalomyelitis’ as it emphasizes the essential encephalitic component of the illness, the muscle pain, and the close clinical and epidemiological similarity to poliomyelitis.

You can read the rest of this interview here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2399326/pdf/postmedj00061-0066.pdf

Source: E. G. Dowsett. Conversation piece. Interview by P. D. Welsby.Postgrad Med J. 1992 Jan; 68(795): 63–65. PMCID: PMC2399326 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2399326/