Right inferior frontal cortex damage impairs the initiation of inhibitory control, but not its implementation

Abstract

Inhibitory control is one of the most important control functions in the human brain. Much of our understanding of its neural basis comes from seminal work showing that lesions to the right inferior frontal cortex (rIFC) increase stop-signal reaction time (SSRT), a latent variable that expresses the speed of inhibitory control. However, recent work has identified substantial limitations of the SSRT method. Notably, SSRT is confounded by trigger failures: stop-signal trials in which inhibitory control was never initiated. Such trials inflate SSRT, but are typically indicative of attentional, rather than inhibitory deficits. Here, we used hierarchical Bayesian modeling to identify stop-signal trigger failures in human rIFC lesion patients, non-rIFC lesion patients, and healthy comparisons. Furthermore, we measured scalp-EEG to detect {beta}-bursts, a neurophysiological index of inhibitory control. rIFC lesion patients showed a more than five-fold increase in trigger failure trials and did not exhibit the typical increase of stop-related frontal {beta}- bursts. However, on trials in which such {beta}-bursts did occur, rIFC patients showed the typical subsequent upregulation of {beta} over sensorimotor areas, indicating that their ability to implement inhibitory control, once triggered, is intact. These findings suggest that the role of rIFC in inhibitory control has to be fundamentally reinterpreted.