Neurochemical abnormalities in chronic fatigue syndrome: a pilot magnetic resonance spectroscopy study at 7 Tesla

• Published in: Psychopharmacology 2022-01, Vol.239 (1), p.163-171
• Main Authors: Godlewska, Beata R., Williams, Stephen, Emir, Uzay E., Chen, Chi, Sharpley, Ann L., Goncalves, Ana Jorge, Andersson, Monique I., Clarke, William, Angus, Brian, Cowen, Philip J.
• Format: Article
• Language: English
• Subjects: Aspartic Acid; Biomedical and Life Sciences; Biomedicine; Brain research; Chronic fatigue syndrome; Cortex (cingulate); Creatine; Development and progression; Fatigue; Fatigue Syndrome, Chronic - diagnostic imaging; Glutathione; Health aspects; Humans; Inositol; Magnetic Resonance Imaging; Magnetic Resonance Spectroscopy; Metabolites; Mitochondria; N-Acetylaspartate; Neurochemistry; Neuronal-glial interactions; Neurosciences; Nuclear magnetic resonance spectroscopy; Original Investigation; Oxidative stress; Pharmacology/Toxicology; Physiological aspects; Prospective Studies; Psychiatry; Spectrum analysis
• ISSN: 0033-3158; 1432-2072
• DOI: 10.1007/s00213-021-05986-6

Rationale Chronic fatigue syndrome (CFS) is a common and burdensome illness with a poorly understood pathophysiology, though many of the characteristic symptoms are likely to be of brain origin. The use of high-field proton magnetic resonance spectroscopy (MRS) enables the detection of a range of brain neurochemicals relevant to aetiological processes that have been linked to CFS, for example, oxidative stress and mitochondrial dysfunction. Methods We studied 22 CFS patients and 13 healthy controls who underwent MRS scanning at 7 T with a voxel placed in the anterior cingulate cortex. Neurometabolite concentrations were calculated using the unsuppressed water signal as a reference. Results Compared to controls, CFS patients had lowered levels of glutathione, total creatine and myo -inositol in anterior cingulate cortex. However, when using N-acetylaspartate as a reference metabolite, only myo -inositol levels continued to be significantly lower in CFS participants. Conclusions The changes in glutathione and creatine are consistent with the presence of oxidative and energetic stress in CFS patients and are potentially remediable by nutritional intervention. A reduction in myo -inositol would be consistent with glial dysfunction. However, the relationship of the neurochemical abnormalities to the causation of CFS remains to be established, and the current findings require prospective replication in a larger sample.