2001 Clinical and Scientific Meeting

McGregor NR [1], De Becker P [2], Clifton Bligh P [3], Stein E [1], Butt HL [1], De Meirleir K [2], Hoskin L [3], Dunstan RH [1], Fulcher G [3], King K [1], Niblett S [1], Roberts TK [1], Dunsmore J [3].

Collaborative Pain Research Unit:
1. Bioanalytical Research Group,
Department of Biological Sciences,
University of Newcastle,
NSW 2308, and
Neurobiology Research Unit
University of Sydney,
Westmead, Australia.;
2. Vrije Universiteit Brussel
Vakgroep Interne Geneeskunde
KRO gebouw niv.
1, Laarbeeklaan 101, 1090
3. Royal North Shore CFS Unit
Royal North Shore Hospital
St Leonards NSW

Evidence based model of the pathogenic mechanisms associated with symptom expression in chronic fatigue syndrome


To retrospectively review the available data to develop a model of the disease processes occurring in CFS.


The medical literature and research finding from the three research groups involved in the presentation were assessed to develop the model. Results: Four factor analysis symptoms groupings are reported to occur in CFS patients: 1) general CFS symptoms, 2) cognitive symptoms, 3) musculoskeletal symptoms, and 4) mood change symptoms (De Becker et al, 2000). The General CFS symptom group consists of the symptoms associated with reactivation of viruses, increased RNase-L fragmentation and infectious symptoms. This group of symptoms represent the cytokine inducing events or predominately pathogen associated events. The cognitive, mood change and musculoskeletal symptoms represent the hosts response or cytokine-mediated symptoms. This is supported by the evidence of therapeutic use of cytokines in treatment of various diseases. In addition to the host based and viral associated symptom patterns are seen co-morbid conditions such as bacterial induced disease and food intolerance that in turn induce changes in the host, which increase morbidity. A model of this complex set of interactions will be presented. The interaction of host and co-morbid disease needs to be understood when CFS patients are assessed and treated.


The infective/cytokine initiating symptoms appear associated with periods of reactivation of the syndrome. The subsequent cytokine mediated host based responses of cognitive, musculoskeletal and mood change symptoms are the bodies response to the syndrome initiators. Reactivation of different viruses is associated with symptom variation whilst the occurrence of co-morbid infections and disease states increase patient morbidity.


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