Chronic fatigue syndrome (CFS) is a complex illness, which is often
misdiagnosed as a psychiatric illness. In two previous reports, using
(1) H MRSI, we found significantly higher levels of ventricular
cerebrospinal fluid (CSF) lactate in patients with CFS relative to those
with generalized anxiety disorder and healthy volunteers (HV), but not
relative to those with major depressive disorder (MDD). In this third
independent cross-sectional neuroimaging study, we investigated a
pathophysiological model which postulated that elevations of CSF lactate
in patients with CFS might be caused by increased oxidative stress,
cerebral hypoperfusion and/or secondary mitochondrial dysfunction.
Fifteen patients with CFS, 15 with MDD and 13 HVs were studied using the
following modalities: (i) (1) H MRSI to measure CSF lactate; (ii)
single-voxel (1) H MRS to measure levels of cortical glutathione (GSH)
as a marker of antioxidant capacity; (iii) arterial spin labeling (ASL)
MRI to measure regional cerebral blood flow (rCBF); and (iv) (31) P MRSI
to measure brain high-energy phosphates as objective indices of
mitochondrial dysfunction. We found elevated ventricular lactate and
decreased GSH in patients with CFS and MDD relative to HVs. GSH did not
differ significantly between the two patient groups. In addition, we
found lower rCBF in the left anterior cingulate cortex and the right
lingual gyrus in patients with CFS relative to HVs, but rCBF did not
differ between those with CFS and MDD. We found no differences between
the three groups in terms of any high-energy phosphate metabolites. In
exploratory correlation analyses, we found that levels of ventricular
lactate and cortical GSH were inversely correlated, and significantly
associated with several key indices of physical health and disability.
Collectively, the results of this third independent study support a
pathophysiological model of CFS in which increased oxidative stress may
play a key role in CFS etiopathophysiology. Copyright © 2012 John Wiley
& Sons, Ltd.
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