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

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The hypothalamus of ME/CFS patients shows functional abnormalities different from those in depressed patients. Our
data suggest that brainstem hypoperfusion in ME/CFS patients could be due to an organic abnormality” (DC Costa
et al; Q J Med 1995:88:767‐773).
1995
“Many neurological diseases produce symptoms of intense fatigue and muscle pain. Abnormalities in cerebral
perfusion were seen on visual reporting of the SPECT images in more than half of the patients with (ME)CFS.
Perfusion defects were not consistently localised to any one region of the brain, being found in the frontal, temporal,
occipital and parietal regions, nor were the defects always unilateral. (ME)CFS is an established, severe and
debilitating illness. We have found visual evidence of cerebral perfusion defects in all regions of the brain. This is
confirmed by the objective quantitative analysis which demonstrates that there is a greater variability in perfusion
pattern of patients with (ME)CFS compared to normal subjects” (J Patterson et al; EOS‐ J Immunol
Immunopharmacol 1995:XV:1‐2:53‐58).
1998
D Di Giuda, G Racciatti et al found that “(ME)CFS is a severely disabling illness. Regional brain perfusion
impairment (mainly hypoperfusion) was found in 83.9% of (ME)CFS patients. This study confirmed
previous reports of brain perfusion impairment in (ME)CFS, providing objective evidence of central nervous
system dysfunction”. (“Brain SPET in Chronic Fatigue Syndrome”: Fourth AACFS International Research &
Clinical Conference, Mass: USA).
2001
Cook DB, Natelson BH et al from the Department of Neurosciences, New Jersey Medical School, reported:
“Some have suggested that (ME)CFS is a ‘functional somatic syndrome’ in which symptoms are inappropriately
attributed to a serious illness. However, brain magnetic resonance imaging (MRI) data suggest that there may be an
organic abnormality associated with (ME)CFS. (Our) results demonstrate that the presence of brain abnormalities in
(ME)CFS are significantly related to subjective reports of physical function and that (ME)CFS subjects with MRI
brain abnormalities report being more physically impaired than those without brain abnormalities” (Int J Neurosci
2001:107(1‐2):1‐6).
2002
A study by Puri et al tested the hypothesis that (ME)CFS is associated with altered cerebral metabolite in the
frontal and occipital cortices and concluded: “Our results suggest that there may be an abnormality of
phospholipid metabolism in the brain in (ME)CFS” (Acta Psychiatr Scand 2002:106(3):224‐226). As Dr Charles
Shepherd, Medical Advisor to the ME Association, commented: “These results add further weight to recently
reported perfusion studies which suggest that there may be pathophysiological abnormalities in the cerebral cortex of
ME/CFS patients” (Co‐Cure MED: 30 th August 2002).
2002
Researchers in Japan (Kuratsune et al) reported that their findings “suggest that the levels of biosynthesis of
neurotransmitters through acetylcarnitine might be reduced in some brain regions of (ME)CFS patients”
(NeuroImage 2002:17(3):1256‐1265).
2003
Using proton magnetic resonance spectroscopy to study the metabolic functions of the basal ganglia in
(ME)CFS patients, Chaudhuri et al reported: “A highly significant increase in the spectra from choline‐containing
compounds was seen in the (ME)CFS patient group” (Neuroreport 2003:14(2):225‐228).