MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME

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greater in (ME)CFS than in the control group (3) The amplitude of MRCP (motor activity‐related cortical potential)
negative potential for tasks was higher in (ME)CFS than the control group. These results clearly show that
(ME)CFS involves altered central nervous system signals in controlling voluntary muscle activities,
especially when the activities induce fatigue. Physical activity‐induced EEG signal changes may serve as
physiological markers for more objective diagnosis of (ME)CFS” (Siemionow V et al. Clin Neurophysiol
2004:115(10:2372‐2381).
2004
The Lancet published a Review entitled “Fatigue in neurological disorders” by Abhijit Chaudhuri et al
(Lancet 2004:363:978‐988). It included (ME)CFS as a neurological disease and it contained 94 references.
2005
In a study looking at grey matter volume reduction in (ME)CFS, researchers found significant reductions in
global grey matter volume in (ME)CFS patients compared with matched controls: “Moreover, the decline in
gray matter volume was linked to the reduction in physical activity, a core aspect of (ME)CFS. These findings suggest
that the central nervous system plays a key role in the pathophysiology of (ME)CFS and point to an objective and
quantitative tool for clinical diagnosis of this disabling disorder” (FP de Langea et al. NeuroImage 2005:26:3:777‐
781).
2005
A News Release from Georgetown University Medical Centre highlighted objective, physiological evidence
that (ME)CFS “can be considered a legitimate medical condition. James Baraniuk, Assistant Professor of
Medicine (said) ‘Our research provides initial evidence that that (ME)CFS and its family of illnesses may be legitimate
neurological diseases and that at least part of the pathology involves the central nervous system’ ”. The
researchers stated: “CFS, Persian Gulf War Illness and fibromyalgia are overlapping symptom complexes.
Neurological dysfunction is common. We assessed cerebrospinal fluid to find proteins that were differentially
expressed in this CFS‐spectrum of illnesses compared to controls. Pooled CFS and (Gulf War Syndrome) samples
shared 20 proteins that were not detectable in the control sample. 62 of 115 proteins were newly described. This pilot
study detected an identical set of central nervous system, innate immune and amyloidogenic proteins in the
cerebrospinal fluids from two independent cohorts of subjects with overlapping (ME)CFS, (Gulf War Syndrome) and
fibromyalgia” (BMC Neurology 2005:5:22).
2007
Professor Julia Newton et al studied the prevalence of autonomic dysfunction in (ME)CFS; she found that
symptoms of autonomic dysfunction were strongly and reproducibly associated with the presence of
(ME)CFS and correlated with severity of fatigue. A particularly strong association was seen with symptoms
of orthostatic intolerance, suggesting that abnormality of dynamic blood pressure regulation is particularly
associated with fatigue severity in ME/CFS, confirming the conclusions of a previous review, and it made
clear that ME/CFS patients are not deconditioned (Q J Med 2007:100:519‐526).
2008
Hoad A and Newton J et al described the prevalence of POTS (postural orthostatic tachycardia syndrome) in
a cohort of patients with ME/CFS and suggest that prevalence may be even higher than shown in the study
results because observations of haemodynamics were limited to just two minutes (some patients were
unable to stand without support and were too unwell to be tested). The authors state: “Studies suggest that
POTS is accompanied with a range of autonomic nervous system abnormalities including vagal withdrawal and
enhanced sympathetic modulation, associated with findings consistent with pooling in the lower limbs. It is important
that (in ME/CFS patients) appropriate investigations are performed. We suggest that at the very minimum this