Abstract
Fatigue can be the primary symptom of a disease itself–this is the case in chronic fatigue syndrome (CFS), which might therefore prove to be a good model for studying the mechanisms underlying fatigue. CFS is an illness characterized by profound disabling and unexplained fatigue sensation lasting at least 6 months resulting in severe impairment in daily functioning and a combination of nonspecific accompanying symptoms including impaired neurocognitive functions such as concentration, attention, and short-time memory. From neuroimaging studies, various neural deteriorations have been shown: for example, patients with CFS had reduced gray-matter volume in the bilateral prefrontal cortex, and within these areas, the volume reduction paralleled the severity of fatigue; the density of serotonin transporters in the brain was significantly reduced in the rostral subdivision of the anterior cingulate; during the fatigue-inducing period, although the functional magnetic resonance imaging (fMRI) responsiveness of task-unrelated brain regions was not changed in healthy subjects, it was attenuated in the CFS patients, and the attenuation speed was correlated with the subjective fatigue sensation. Although the neural deterioration in fatigue has mostly been studied for this specific disorder, prolonged or accumulated fatigue may introduce both functional and organic deteriorations of central nervous system among healthy population. [J Physiol Sci. 2008;58 Suppl:S19]
