Anxious arousal alters prefrontal cortical control of stopping
Using magnetoencephalography to investigate the relationship between induced anxiety and stopping during a stop‐signal task, increased prefrontal beta‐band activity was related to successful stopping, with beta in right inferior frontal gyrus correlated with stopping efficiency. Anxiety slowed stop‐signal reaction times and weakened prefrontal beta (which no longer correlated with SSRT), suggesting altered right IFG functioning might explain impaired inhibitory control during anxious arousal.
Anxiety heightens vigilance and stimulus‐driven attention to the environment, which may in turn disrupt cognitive control processes such as response inhibition. How this unfolds at the neural level is unclear. Previous evidence implicates the right inferior frontal gyrus (IFG) as an important cortical node in both stimulus‐driven attention and inhibitory control. Here we used magnetoencephalography (MEG) to investigate the neural mechanisms involved in the relationship between threat‐induced anxiety and stopping during a stop‐signal task, where a visual go signal was occasionally followed by an auditory stop signal. Healthy individuals (N = 18) performed the task during the threat of unpredictable shocks and safety to modulate anxious arousal. Behaviorally, we observed that stopping was impaired during threat (i.e. slower estimated stop‐signal reaction times), indicating that anxious arousal weakens inhibitory control. MEG source analyses revealed that bilateral IFG and right dorsal prefrontal cortex showed increased beta‐band activity (14–30 Hz) to the stop signal that varied as a function of successful stopping during nonanxious (safe) conditions only. Moreover, peak beta‐band responses from right IFG were inversely correlated with stopping efficiency during nonanxious conditions. These findings support theoretical claims that beta oscillations function to maintain the current sensorimotor state, and that the lack of differential beta‐band activity in prefrontal cortices underlies anxiety‐related deficits in inhibitory control. We specifically argue that altered right IFG functioning might directly link impaired cognitive control to heightened stimulus‐driven responding in anxiety states.