In yet another fascinating article Cort Johnson explores the work of Japanese scientists into the way fatigue is produced in the brain and the body.
Thus, there are two parts to centrally produced fatigue. There is the facilitation process that allows us to activate the motor cortex and recruit more muscles in the face of fatigue, and there is the inhibition system that stops the facilitation system in its tracks. The second of these is in control in ME/CFS.
They forward the hypothesis that damage to the prefrontal cortex is a causative factor in the abnormal fatigue of people with ME.
The Japanese researchers zeroed in on the dorsolateral prefrontal cortex (DLPFC), a part of the brain that regulates of a variety of functions often impaired in ME/CFS including sensory inputs (physical sensations, over-stimulation), emotions (high emotional lability), attention span (attention what?), working memory (“please repeat that”), planning (right!), self-control (highly needed) and decision-making (agonizing). It’s the seat of executive functioning, which studies suggests is not going so well in Chronic Fatigue Syndrome.
Cognitive processes are what the prefrontal cortex is known for, but that’s not why these researchers are zeroing in on it; it also plays an important role in motor control; i.e., movement. The DLPFC connects to several parts of the brain that regulate movement including the premotor cortex, supplementary motor area, cerebellum, and basal ganglia.
Because the dorsal lateral prefrontal cortex appears to decide which process – energy enhancement or the induction of fatigue – is going to prevail, the authors hypothesize that metabolic, functional, or structural damage to this part of the brain is key to the development of fatigue in Chronic Fatigue Syndrome.