Cerebral glucose metabolism in patients with chronic fatigue syndrome

pattismith

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(old study, but wasn't available on PR)


Observer independent analysis of cerebral glucose metabolism in patients with chronic fatigue syndrome
2003
Siessmeier T1, Nix WA, Hardt J, Schreckenberger M, Egle UT, Bartenstein P.
1Department of Nuclear Medicine, Johannes Gutenberg University, Mainz, Germany. siessmeier@nuklear.klinik.uni-mainz.de
Abstract

OBJECTIVES:
To evaluate cerebral glucose metabolism, assessed by 18-fluorodeoxyglucose positron emission tomography (FDG-PET), in patients with chronic fatigue syndrome (CFS), using an observer independent analytical approach; and to characterise any observed alterations by correlating them with neuropsychological deficits.
METHODS:
26 patients (13 female, 13 male) were examined. They all fulfilled the CDC diagnostic criteria for CFS. Their ages ranged from 26 to 61 years (mean (SD) age, 43 (9.3) years). They underwent extensive psychometric testing including the hospital anxiety and depression scale (HADS) and the short form 36 item health questionnaire (SF-36). Brain FDG-PET was done in all the subjects. After stereotactic normalisation, single subject comparisons with an age and sex matched normal database (n = 18) and a group comparison between the patients and normal controls were undertaken, along with additional correlation analyses between brain metabolism and psychometric test scores.

RESULTS:
12 of the 26 patients showed no significant decrease in FDG uptake compared with the controls. Of the remaining 14, 12 showed hypometabolism bilaterally in the cingulate gyrus and the adjacent mesial cortical areas. Five of these 12 patients also had decreased metabolism in the orbitofrontal cortex. The two remaining patients had hypometabolism in the cuneus/praecuneus. Correlation analyses showed significant correlations between some test scores (anxiety, depression, health related quality of life) but not fatigue and regional reductions in glucose metabolism.

CONCLUSIONS:
Although abnormalities in FDG-PET were only detectable in approximately half the CFS patients examined, and no specific pattern for CFS could be identified, PET may provide valuable information in helping to separate CFS patients into subpopulations with and without apparent alterations in the central nervous system.
 

pattismith

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RESULTS:
12 of the 26 patients showed no significant decrease in FDG uptake compared with the controls.

Of the remaining 14, 12 showed hypometabolism bilaterally in the cingulate gyrus and the adjacent mesial cortical areas.

Five of these 12 patients also had decreased metabolism in the orbitofrontal cortex.

The two remaining patients had hypometabolism in the cuneus/praecuneus.

Correlation analyses showed significant correlations between some test scores (anxiety, depression, health related quality of life) but not fatigue and regional reductions in glucose metabolism.
in another study on cerebral blood flow on myotonic dystrophy (DM1) and proximal myotonic myopathy (PROMM= DM2), they found:
"PET studies in PROMM/DM2 patients showed a bilateral decrease in regional cerebral blood flow (rCBF) of the orbitofrontal and medial frontal cortex,
whereas DM1 patients had more widespread hypoperfusion that extended to the dorsolateral frontal cortex and subcortical regions.
conclusion is: "Impaired visual-spatial function may be present in proximal myotonic myopathy (DM2). This correlates best with a reduction in regional cerebral blood flow observed in H2(15)O PET brain scans"

I wonder if the CFS subgroup with impaired metabolism in the orbitofrontal cortex has similar visual-spacial function alteration as DM2 patients...
 
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andyguitar

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The theory of Type 3 diabetes is that insulin resistance in the brain is a cause of Alzheimers. There is a decreased ability to metabolise sugar in the brain in Alzheimers but it does not prove that it is the cause. Might just be an effect. As Alzheimers is not reversible but me/cfs is I dont think they have that much in common when it comes to the cause. But the possibility that the neurological problems in me/cfs could be caused by a local defect in sugar metabolism is something worth considering for the open minded.
 
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Not sure but I think intranasal insulin can help in this area;
From what i've read about this it's an alternative way of delivering insulin but not something that was designed to raise insulin levels in the brain directly but has been found to do so. It also raises levels in the brain without leading to dangerously high levels in the blood which would be the result of taking insulin by the other routes.
 
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