463 Beta Power in the Ventral Intermediate Nucleus of the Thalamus Predicts Slowing Effect of High-Frequency Stimulation on Response Inhibition in Essential Tremor Patients

INTRODUCTION: Action control may be impaired in essential tremor (ET). Disruptions in cerebello-thalamo-cortical networks are thought to underlie deficits in response inhibition, and previous studies have shown that beta band oscillations in the ventral intermediate nucleus (VIM) of the thalamus suppress behaviorally irrelevant information. While deep brain stimulation (DBS) targeting the VIM is a common treatment option for ET motor symptoms, the neurophysiology of how high-frequency stimulation interacts with inhibitory processes remains unknown. METHODS: Nine ET patients undergoing awake VIM DBS surgery with microelectrode recordings participated in this study. Subjects completed a stop-signal task where an arrow appeared on a screen, prompting subjects to quickly press a button in the presented arrow’s direction. In 25% of trials, the arrow turned purple after a delay, serving as a stop-signal for subjects to inhibit their response. Six subjects completed an additional block of the task during which the VIM was stimulated at 130 Hz for one second preceding stop-signal presentation. We correlated power changes during non-stimulated blocks with subjects’ stop-signal reaction-times (SSRTs), or the latency to successfully stop a response, across blocks. RESULTS: VIM beta (12–35 Hz) power was significantly higher during successful response inhibition compared to failed inhibitions. Increased high beta (20–35 Hz) power correlated with longer SSRTs, or slower inhibition, during non-stimulated blocks. Higher low beta (12–20 Hz) power during response inhibition corresponded with a greater SSRT increase following stop-signal stimulation relative to non-stimulated SSRTs. CONCLUSIONS: Increased VIM beta power during response inhibition is associated with slower inhibition and predicts further slowing following high-frequency VIM stimulation. Beta power in the VIM could thus potentially serve as a biomarker for impaired inhibitory efficiency, which could inform adaptive neuromodulation strategies for ET motor and cognitive symptoms.