Editor’s Comment: One of the objections raised against using the name “myalgic encephalomyelitis” is that inflammation (“-itis”) in the central nervous system (“encephalo”) could not be proven. In this study, the researchers measured the presence of a protein in the brain that is released by microglia when they are activated. Microglia are the first line of immune defense in the central nervous system, which means microglial activation is an indicator of inflammation. Chronic activation of microglia can lead to excitotoxicity, a mechanism that has been proposed for both Gulf War Illness and Autism (Blaylock, “Chronic Microglial Activation and Excitotoxicity Secondary to Excessive Immune Stimulation: Possible Factors in Gulf War Illness and Autism”). Excitotoxicity has been put forth as a mechanism of ME/CFS by a number of clinicians and researchers, including Drs. Paul Cheney, Jay Goldstein, Morris and Maes, Martin Pall, and, most recently, Jarred Younger.
Neuroinflammation in Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis: An 11C-(R)-PK11195 PET Study.
By Y. Nakatomi et al.
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Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a disease characterized by chronic, profound, disabling, and unexplained fatigue. Although it is hypothesized that brain inflammation is involved in the pathophysiology of CFS/ME, there is no direct evidence of neuroinflammation in patients with CFS/ME. Activation of microglia or astrocytes is related to neuroinflammation. 11C-(R)-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinoline-carboxamide (11C-(R)-PK11195) is a ligand of PET for a translocator protein that is expressed by activated microglia or astrocytes. We used 11C-(R)-PK11195 and PET to investigate the existence of neuroinflammation in CFS/ME patients.
METHODS: Nine CFS/ME patients and 10 healthy controls underwent 11C-(R)-PK11195 PET and completed questionnaires about fatigue, fatigue sensation, cognitive impairments, pain, and depression. To measure the density of translocator protein, nondisplaceable binding potential (BPND) values were determined using linear graphical analysis with the cerebellum as a reference region.
RESULTS: The BPND values of 11C-(R)-PK11195 in the cingulate cortex, hippocampus, amygdala, thalamus, midbrain, and pons were 45%-199% higher in CFS/ME patients than in healthy controls. In CFS/ME patients, the BPND values of 11C-(R)-PK11195 in the amygdala, thalamus, and midbrain positively correlated with cognitive impairment score, the BPND values in the cingulate cortex and thalamus positively correlated with pain score, and the BPND value in the hippocampus positively correlated with depression score.
CONCLUSION: Neuroinflammation is present in widespread brain areas in CFS/ME patients and was associated with the severity of neuropsychologic symptoms. Evaluation of neuroinflammation in CFS/ME patients may be essential for understanding the core pathophysiology and for developing objective diagnostic criteria and effective medical treatments.
Source: Nakatomi Y, Mizuno K, Ishii A, Wada Y, Tanaka M, Tazawa S, Onoe K, Fukuda S, Kawabe J, Takahashi K, Kataoka Y, Shiomi S, Yamaguti K, Inaba M, Kuratsune H, Watanabe Y. J Nucl Med. 2014 Mar 24. [Epub ahead of print]