Not available yet in English but a quick translation of the extended Japanese abstract gives-
Not too much info here but it is the introduction in full
In our study using PET scanning, hyoperfusion and low synthesis in the frontal lobe, cingulate gyrus, temporal and occipital cortex, basal ganglia, hippocampus of acetylcarnitine- mediated neurotransmitters such as glutamate, aspartic acid, aminobutyrl acid, has been reported,
There was a decrease in serotonin transporter density in the anterior cingulate gyrus, and in particular the serotonin transporter density in the intermediate region of of the cingulate gyrus had a negative correlation with the pain score. Furthermore, in MRI studies, the volume reduction level of bilateral prefrontal cortex correlated with severity of fatigue.
Dysfunction of the central nervous system is considered to be the cause of fatigue even in tother fatigue-related neurological deseases such as multiple sclerosis, Parkinson's disease, post polio fatigue synrome, etc.
Neuroinflammation in the cerebrum is thought to be the cause of disease progress. It is suggested that it is involved. There are reports that the level of inflammatory cytokines of peripheral blood and cerebrospinal fluid which may be indicative of neuroinflammation in the brain are higher in the ME/CFS patient group than in the healthy contol group.
However, in order to clarify the presence of intracerebral neuritis and its involvement in the pathophysiology of ME/CFS, we evaluated intracerebral neuroinflammation directly using imaging techniques such as PET, it is necessary to investigate the relationship with the severity of symptoms (?).
Neuroinflammation in the brain can be visualized by observing activation of microglia or astrocytes.