基底核の脳卒中後疲労における重要な役割：パイロットスタディ

This pilot study aimed to explore the neural mechanisms underlying cognitive fatigue (CF) in stroke survivors, with a focus on the role of basal ganglia damage. Sixteen participants were recruited, including six stroke survivors with basal ganglia lesions (BG+), four with lesions elsewhere in the brain (BG-), and six healthy controls (HC). Participants underwent neuropsychological assessments and an fMRI fatigue induction task, where CF was induced using a modified letter-comparison task under individually titrated response deadlines. CF was assessed using the Visual Analog Scale of Fatigue (VAS-F), and fMRI data were analyzed to identify task-evoked activation within the fatigue network. Stroke survivors reported higher levels of CF compared to healthy controls, with the BG+ group exhibiting the highest fatigue levels and the greatest increase in fatigue over time. The BG+ group also demonstrated the most pronounced disparity in reaction times between short and long response deadlines. Functional neuroimaging revealed that CF ratings correlated with task-evoked activation in the fatigue network, but only in the BG- group. Our findings suggest that while stroke presence generally may increase CF, damage specifically involving the basal ganglia accelerates its accrual. Moreover, the ability to engage the fatigue network may mitigate fatigue, as observed in the BG- group. These results underscore the importance of basal ganglia in understanding CF and highlight the need for future research in this area.