Journal of IiME Volume 2 Issue 1 www.investinme.org WHO GETS ME AND WHY - The role of impaired capillary blood flow in ME (continued) pathophysiologies for either diagnosis. To a large extent this is the current situation. For example, a 2001 English publication titled “What is ME? What is CFS?” (1) discussed ME mainly in terms of the findings of American investigators, only a 1981 paper by Ramsay was quoted and no reference was made to either edition of his book. In 2007, The Nightingale Research Foundation published, “The Nightingale myalgic encephalomyelitis definition,” (2) even though in their 1992 book, Dr.Hyde had suggested that “encephalopathy” was a more appropriate term. Primary ME was defined as, “…an acute onset biphasic epidemic or endemic (sporadic) infectious disease process where there is always measurable and persistent diffuse vascular injury of the CNS in both the acute and chronic phases. Primary ME is associated with immune and other pathologies.” The concept of “…persistent diffuse vascular injury,” would rule out any involvement of Ramsay-style remissions. It is clear that the possible role for shapechanged red cells as recorded in my paper in the 1992 book, was rejected. At a meeting of Canadian and American investigators who were interested in ME, a consensus was reached and released as the Canadian Consensus. In 2007, a review was published under the title, “Definitions and aetiology of myalgic encephalomyelitis: how the Canadian consensus clinical definition of myalgic encephalomyelitis works.”(3) It was noted, “To improve clinical observation, the Canadian definition and diagnostic protocol lays out several regions of pathophysiological dysfunction, as necessary components of the syndrome of myalgic encephalomyelitis, but the particular expression of symptoms within each region is contingent between individuals and their particular pattern is left open to be decided by clinical observation of the individual and later diagnostic classification.” of the writing, but the enclosed message is far from clear. It was noted also, that, “The possible aetiology of myalgic encephalomyelitis is under scientific observation. This is done by experiment and by controlled observation. Many observers are following various lines of investigation and observation as to the aetiology of myalgic encephalomyelitis, which we are following with interest.” This statement seems not to recognise that ME has been studied for 50 years. like is being compared with like. The crucial factor is whether or not Given the degrees of difference in the various definitions, there seems to be a grave danger that apples are being compared to oranges. In general, two features of the paper stand out. No mention was made of Ramsay’s work or of remissions and there was no indication that blood flow was a problem. Therefore it seems that because of the conflicting views of experts and a general lack of agreement concerning the aetiology and pathophysiology of ME, a small section of the community will continue to suffer a reduced quality of life while experiencing a variety of symptoms, which, if Invest in ME (Charity Nr. 1114035) they are lucky may disappear for variable periods of time during remissions. WHO IS AT RISK OF DEVELOPING ME? In any group of people who suffer from the same viral infection, most return to full health in less than 14 days, while a small proportion become chronically unwell. This implies that those who continue to be unwell (?ME people) are different from the normal population in some feature. About the time I became involved with ME in 1983, I was developing an interest in the measurement of blood viscosity and blood filterability. Control Initially I studied blood samples from the blood donor panel, but through the good offices of Prof.J.C.Murdoch, who had a clinical interest in ME, I obtained blood samples from 21 female and 11 male patients with ME. samples were obtained from age and gender matched blood donors. Blood viscosity was measured at four shear rates and blood was filtered through polycarbonate filters with 5 micron pores at four levels of negative pressure. The results were published in 1986 (4) and showed that although there were differences in the results from blood viscometry of ME people and controls, they did not reach statistical significance. In contrast, at the lowest filtration pressure, the values for ME females were significantly different from controls, (an indication of stiffened red cells) but the differences in the male values did not reach significance. An examination of the data revealed that some ME values were near normal and would have influenced the results. The implications of the results were that ME This 59 word sentence is typical people could be at risk of blood flow problems in the microcirculation because of the effects of poorly deformable red cells. It should be noted that for the assessment of filterability, EDTA-anticoagulated blood was used and filtration took place within half an hour of the sample being drawn. Subsequent developments from the simple technique included the washing of the red cells in saline, but such treatment greatly changed blood filterability. Our report concluded, “ … advances in our understanding of the aetiology of the disorder will come from investigations in the acute phase, and blood rheology may be of value in identifying those who are acutely affected.” Although non-ME subjects may have poorly filterable blood for 12 to 14 days after an infection, ME blood remains poorly filterable as long as they are symptomatic. So ME people respond to agents which change the internal environment, by stimulating change in red cell shape and making them less deformable, probably because of a persisting, but unidentified factor in the blood. As will be discussed later, that factor has the capacity to switch off, resulting in a remission. Until the factor has been identified, it seems inappropriate to (Continued on page 26) Page 25/34
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