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

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includes haemodynamic assessment in response to standing of patients attending CFS/ME clinical services” (Q J Med
September 2008:doi:10.1093/qjmed/hcn123).
2009
Newton et al demonstrated that lower blood pressure and abnormal diurnal blood pressure regulation
occur in patients with ME/CFS and considered the links between hypotention and fatigue. The authors
concluded: “Compared with the control population, the (ME)CFS group had significantly lower systolic blood
pressure and mean arterial blood pressure and exaggerated diurnal variation. There was a signficant inverse
relationship between increasing fatigue and diurnal variation of blood pressure in the (ME)CFS group. This study has
further consolidated the evidence that lower blood pressure occurs in (ME)CFS and that…lower night‐time blood
pressure seems to be a significant problem that may lead to enhanced diurnal variation in blood pressure that associates
with fatigue. We and others have previously demonstrated that autonomic nervous system function is significantly
impaired in (ME)CFS. We would suggest that…one mechanism whereby abnormalities in autonomic function may be
manifest clinically is through blood pressure dysregulation” (Psychsom Med 2009:71:
doi:10.1097/PSY.0b013e31819ccd2a).
Documented abnormalities shown on neuroimaging in ME/CFS
As reported by Dr John Breward as long ago as 2001 in the Newsletter of The 25% ME Group, Issue 11: “The
cumulative evidence is now incontestable: there are measurable physical abnormalities in the brain in
ME”.
1992
“(ME)CFS is a severely disabling illness. Compared to the normal control group, the (ME)CFS group showed
significantly lower cortical / cerebellar rCBF (regional cerebral blood flow) ratios throughout multiple brain regions.
SPECT provided objective evidence for functional impairment of the brain in the majority of the (ME)CFS subjects.
The central nervous system dysfunction in (ME)CFS may be a primary phenomenon or it may be secondary to
undefined systemic factors. The majority of (ME)CFS subjects studied showed SPECT scan abnormalities providing
objective evidence of central nervous system dysfunction in (ME)CFS” (M Ichise et al; Nuclear Medicine
Communications 1992:13:767‐772).
1994
“We compared SPECT scans of patients with (ME)CFS with those of patients with ADC (AIDS dementia complex)
and unipolar depression. The MCUI (midcerebral uptake index) was signficantly different across all groups. This
study demonstrates that (ME)CFS shares some similarities on SPECT imaging with both ADC and unipolar
depression. The MCUI was significantly lower in patients with (ME)CFS and ADC than in patients with major
unipolar depression or the healthy comparison group. By this objective standard, the pathophysiologic process in the
central nervous system of patients with (ME)CFS would seem to be more similar to that in patients with ADC than to
patients with unipolar depression. Moreover the MCUI values correlated with the regional defect count in the
(ME)CFS and ADC groups, but not in the depressed patients or control subjects” (Schwartz RB et al; American
Journal of Reontgenology 1994:162:943‐951).
1995
“We looked for brain perfusion abnormalities in patients with ME/CFS. Hypoperfusion of the brainstem was marked
and constant. Brainstem hypoperfusion was confirmed in all ME/CFS patients. Patients with ME/CFS have a
generalised reduction of brain perfusion, with a particular pattern of hypoperfusion of the brainstem. Brainstem
hypoperfusion appears to be the differentiating factor between our ME/CFS patients and those with major depression.