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) Because tiredness is a major problem for those who suffe from multiple sclerosis, (MS) at the conclusion of our 1986 study on ME, we investigated the filterability and other aspects of blood samples from members of the local Multiple Sclerosis Society. As with ME, the rate of blood filterability was much less than that of healthy controls and there were changes in red cell morphology. A possibly relevant implication of these changes is that in 1983, Swank et al (23) had shown by xenon washout that in MS subjects, “…there occurred a progressive, generalised decrease in cerebral blood flow and in red cell delivery with age, which was significantly greater than observed in normal subjects. The rate of decrease in cerebral blood flow and red cell delivery correlated directly with the rate of progress of the disease. Studies using single photon computed tomography (SPET or SPECT) have shown in other conditions with shape-changed red cells, that there can be significant reductions in regional cerebral blood flow. The relevance of this is that on March 30 1994, Dr.D.C.Costa presented his findings from a SPET study of ME patients at the annual general meeting of the British Nuclear Medicine Society. He reported that ME/CFS patients, “… had a generalised reduction in brain perfusion, “ and that, “… brainstem blood flow was significantly lower than in patients with depression and that both patient groups had significantly lower brainstem blood flow than in healthy subjects.” Even though I had published three reports concerning the effects of nondiscocytic red cells in ME patients prior to 1994, Dr.Costa hypothesised that the reduced demand for oxygen in the brain related to an overactive immune system which resulted in an excessive production of cytokines. Dr.Costa’s comparison of the cerebral blood flow of ME/CFS with depression draws attention to a significant literature concerning SPECT scans and depression. Perhaps the most informative was a study by Bench et al (24) which showed that a region of the brain with impaired blood flow during depression, showed normal blood flow rates when the depressive episode resolved. Evidently the regions associated with reduced blood flow have diagnostic significance as shown in another study by Dr.Costa. Lucey, Costa et al (25) reported that in some psychiatric disorders, there were significant differences in regional cerebral blood flow, as defined by SPET. While whole brain blood flow correlated with anxiety, there were significant regional cerebral blood flow differences between patients with obsessive compulsive disorder and post-traumatic stress disorder and controls. REMISSIONS – THE CORNER STONE OF RAMSAY’S CONCEPT OF ME. Even though Ramsay had described remissions as a feature of ME, and gave examples of the Invest in ME (Charity Nr. 1114035) remission/relapse cycle, remissions are unrecognised by American investigators and are little recognised in other countries. This situation could be a possible consequence of ME being considered as the result of a persistent infection or a persistent immunological abnormality, or the consequence of localised pathology, as such beliefs would be incompatible with the remissions which Ramsay recorded. My first experience with a remission related to a young woman who delivered a blood sample about 9am one morning. She explained that she had been too unwell to have had a blood sample taken earlier. On checking the details on her blood test request form it was noted that she had checked the box ‘well with no symptoms.’ pointed out that if she was well when she had the blood drawn then it was likely that the results would be normal. About 4pm on the same day she returned with another blood sample. She had ‘crashed’ about 3.30pm, for no discernible reason, and gone to the laboratory for another sample. The request form was marked ‘severely unwell.’ When the samples had been assessed it was found that the morning sample was normal and the afternoon sample was grossly abnormal. What factor or factors switch off to restore red cell shape populations to normal with improved wellbeing, and switch on to become symptomatic with changed red cell shape populations, remain unknown. However, the observation is consistent with Ramsay’s comment that during remission muscle function returns to normal. Those observations led to an attempt to gain some insight into the frequency of remissions and concomitant changes in ME people in New Zealand. A panel of 37 females and 11 males who had been diagnosed by a physician as having ME at least 2 years previously, gave informed consent to take part in a 40 week-long study. At commencement and at four-weekly intervals thereafter, the panel met to record their symptoms and level of wellbeing and to provide a 5-drop sample of venous blood for red cell shape analysis. A total of 519 blood samples (401 female, 118 male) were assessed. While the majority of blood samples showed the increased flat cells of chronic ME, normal results occurred sporadically. At one extreme there were five women who were unwell and had abnormal blood tests in 11 of 11 blood samples. Because of the four-week space between samples it is not known if remissions had occurred in the interval or if the women were in the group noted by Ramsay, who did not have remissions. At the other extreme was a woman who was well, with normal blood tests in 6 of 11 samples. The most frequent result, for both sexes, was to have two remissions during the 40 weeks of the study. The findings led to the conclusion that remissions were not uncommon events. (Continued on page 30) Page 29/34
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