Dynamic Causal Modelling Highlights the Importance of Decreased Self-Inhibition of the Sensorimotor Cortex in Motor Fatigability

Abstract

Motor fatigability emerges when challenging motor tasks must be maintained over an extended period of time. It is a frequently observed phenomenon in everyday life which affects patients as well as healthy individuals. Motor fatigability can be measured using simple tasks like finger tapping at maximum speed for 30s. This typically results in a rapid decrease of tapping frequency, a phenomenon called motor slowing. In a previous study (Bachinger et al. 2019), we showed that motor slowing goes hand in hand with a gradual increase of activation in the primary sensorimotor cortex (SM1), supplementary motor area (SMA), and dorsal premotor cortex (PMd). Previous electrophysiological measurements further suggested that the increase in SM1 activity might reflect a breakdown of inhibition and, particularly, a breakdown of surround inhibition which might have led to heightened coactivation of antagonistic muscles. It is unclear what drives the activity increase in SM1 caused by motor slowing and whether motor fatigability affects the dynamic interactions between SM1 and upstream motor areas like SMA and PMd. Here, we performed dynamic causal modelling to answer this question. Our main findings revealed that motor slowing was associated with a significant reduction in SM1 self-inhibition which is in line with previous electrophysiological results. Additionally, the model revealed a significant decrease in the driving input to premotor areas suggesting that structures other than cortical motor areas might cause motor fatigability.