As you might expect, the journal Medical Hypotheses publishes speculative papers about the cause and consequences of diseases. Because it is an ‘orphan illness of unknown aetiology’, ME/CFS has been the subject of a number of such papers over the years, most recently a contribution on the possible role of brain inflammation. Dr Simon Arnett and colleagues at the Australian National University speculate that the long-term presence of inflammatory substances (mediators) within the central nervous system and brain leads to both neurological dysfunction and patients’ symptoms. It may be, for example, that ME/CFS patients have a relative immunodeficiency, such that infections, which are poorly controlled at an early stage, lead to chronic inflammatory responses.
The authors say their theory provides an explanation for the known range and pattern of symptoms seen in ME/CFS, such as the neurological and endocrine changes. Of course, the hypothesis that ME/CFS is a disease of long-term inflammatory processes of the brain raises the question of whether centrally-acting anti-inflammatory treatments might be effective. The authors have particular interest in the use of biological agents against TNF (an inflammatory mediator). These anti-TNF agents have been used with some success for Alzheimer’s disease – another condition in which a neuroinflammatory mechanism is increasingly implicated – and could possibly have a role in ME/CFS too.
Reference: Chronic fatigue syndrome – a neuroimmunological model. Arnett SV, et al. Med Hypotheses 2011 Jul; 77(1): 77-83.