ME Research is suffering from inaccurate diagnosis
Authors
Janice Storey and Margaret Williams
Publication
Biologist 2003; 50(3): 104
Summary
Research into the lifelong, uniquely disabling illness, myalgic encephalomyelitis (ME), is in danger due to the illness regularly being redefined and subsumed under the label of ‘Chronic Fatigue Syndrome’ (CFS). CFS is a non-specific term for a heterogeneous patient population suffering from various syndromes of chronic fatigue, whether organic or psychiatric in nature, only one of which is ME. These inappropriate re-definitions give the inaccurate impression that all syndromes of chronic fatigue have a psychiatric aetiology, whereas ME has been formally classified in the International Classification of Diseases (ICD) by the WHO as a neurological disorder since 1969. No one, however, disputes that, as in all serious illness, some sufferers may exhibit psychological morbidity, including emotional lability.
Accurate disease diagnosis and classification are essential for real progress to be made in understanding ME, and it must not be confused with non-specific states of ongoing, medically unexplained, fatigue. The latter are classified in the ICD under Mental and Behavioural disorders at section F48.0, a category from which ME is expressly excluded. Confusingly, however, ‘chronic fatigue syndrome’ is listed in the ICD as a term by which ME is also known, and the international research community now use the term CFS instead of ME. Unhelpfully, some UK psychiatrists who specialise in chronic fatigue refer to medically unexplained fatigue as ‘CFS’ without differentiation, so it is imperative to be aware that the term ‘CFS’ can mean different things to different people…
To this end, there is an ever-increasing body of evidence from international centres of excellence for a variety of biomarkers for ME. These exist, for not only neurological deficits, as demonstrated by nuclear medicine techniques such as SPECT and MRS scans (which demonstrate cerebral hypoperfusion), but also for endocrine dysfunction (disturbance of the HPA axis), immune dysfunction (evidence of an unusual and inappropriate immune response), and vascular disturbance (evidence of disrupted biology of blood vessel endothelium), together with evidence of mitochondrial abnormalities in muscle…
For example, at the recent AACFS conference in Virginia, USA (2003), Scottish researchers Drs Vance Spence and Gwen Kennedy (Vascular Diseases Research Unit, Dundee) presented novel findings of a prolonged action of acetylcholine in the microvasculature and of increased plasma isoprostanes as markers of oxidative stress in ME/CFS. In addition, they showed evidence of increased neutrophil apoptosis (programmed early cell death) in ME/CFS and higher levels of TGF b1, which may be indicative of a persistent viral infection or a toxic state. Of special significance is the work of Professor Robert Suhadolnick (Temple University, Philadelphia, USA), who gave an excellent overview of the many biological and biochemical processes which are known to be altered and implicated in the pathoaetiology of ME/CFS, including: oxidative stress (nitric oxide / peroxynitrite); 2,5A synthetase / RNase L; p68 kinase (PKR); the mechanisms involved in apoptosis; skeletal muscle function; mitochondrial function; and brain metabolism. Indeed, the abnormal 2,5A synthetase/ RNase L pathway may soon be regarded as a diagnostic test for the disorder. A full report on this conference can be viewed at www.meresearch.org.uk.
Much more work needs to be undertaken to build upon these findings in order to better understand the aetiology of ME and isolate potential treatment strategies. The UK ME community, however, is aware that certain important grant awarding bodies are apparently ignoring the large body of international biomedical evidence of serious organic pathology in ME, prefering to allocate research funding to re-evaluate the effectiveness of psychological management strategies more appropriate to aberrant illness belief. It is our view that future funded ME research should proceed along well-established biological routes — to do anything else would not only be misleading but would waste the already limited funds.
