The ability to adapt to aversive stimuli is critical for mental health. Here, we investigate the relationship between habituation to startling stimuli and startle-related activity in medial frontal cortex as measured by EEG in both healthy control participants and patients with Parkinson disease (PD). We report three findings. First, patients with PD exhibited normal initial startle responses but reduced startle habituation relative to demographically matched controls. Second, control participants had midfrontal EEG theta activity in response to startling stimuli, and this activity was attenuated in patients with PD. Finally, startle-related midfrontal theta activity was correlated with the rate of startle habituation. These data indicate that impaired startle habituation in PD is a result of attenuated midfrontal cognitive control signals. Our findings could provide insight into the frontal regulation of startle habituation.

pFC is proposed to implement cognitive control via directed “top–down” influence over behavior. But how is this feat achieved? The virtue of such a descriptive model is contingent on a mechanistic understanding of how motor execution is altered in specific circumstances. In this report, we provide evidence that the well-known phenomenon of slowed RTs following mistakes (post-error slowing) is directly influenced by the degree of subthalamic nucleus (STN) activity. The STN is proposed to act as a brake on motor execution following conflict or errors, buying time so a more cautious response can be made on the next trial. STN local field potentials from nine Parkinson disease patients undergoing deep brain stimulation surgery were recorded while they performed a response conflict task. In a 2.5- to 5-Hz frequency range previously associated with conflict and error processing, the degree phase consistency preceding the response was associated with increasingly slower RTs specifically following errors. These findings provide compelling evidence that post-error slowing is in part mediated by a corticosubthalamic “hyperdirect” pathway for increased response caution.