Novelty-induced frontal-STN networks in Parkinson's disease

Novelty detection is a primitive subcomponent of cognitive control that can be deficient in Parkinson's disease (PD) patients. Here, we studied the corticostriatal mechanisms underlying novelty-response deficits. In participants with PD, we recorded from cortical circuits with scalp-based electroencephalography (EEG) and from subcortical circuits using intraoperative neurophysiology during surgeries for implantation of deep brain stimulation (DBS) electrodes. We report three major results. First, novel auditory stimuli triggered midfrontal low-frequency rhythms; of these, 1-4 Hz delta rhythms were linked to novelty-associated slowing, whereas 4-7 Hz theta rhythms were specifically attenuated in PD. Second, 32% of subthalamic nucleus (STN) neurons were response-modulated; nearly all (94%) of these were also modulated by novel stimuli. Third, response-modulated STN neurons were coherent with midfrontal 1-4 Hz activity. These findings link scalp-based measurements of neural activity with neuronal activity in the STN. Our results provide insight into midfrontal cognitive control mechanisms and how purported hyperdirect frontobasal ganglia circuits evaluate new information.

Automated summary

This study investigates the corticostriatal mechanisms underlying novelty-response deficits in Parkinson's disease (PD) patients. The results suggest that novel auditory stimuli trigger specific low-frequency rhythms, where 1-4 Hz delta rhythms are associated with slowing response and 4-7 Hz theta rhythms are attenuated in PD patients. Moreover, subthalamic nucleus (STN) neurons show response modulation and coherence with midfrontal 1-4 Hz activity, indicating the involvement of hyperdirect frontobasal ganglia circuits in evaluating new information.