152 Caudate and Dorsolateral Prefrontal Cortex Beta Bursts During Working Memory Encoding Correlate with Memory Impairment in Parkinson’s Disease

Abstract

INTRODUCTION: Cognitive dysfunction is a common nonmotor symptom of Parkinson’s disease (PD), with memory impairment being a primary cause of disability. Decreased dopamine in PD elevates beta power in cortico-striato-thalamo-cortico (CSTC) motor circuits and is the basis of closed-loop deep brain stimulation (DBS) strategies. Analogous dysfunction of parallel CSTC cognitive circuitry including caudate and dorsolateral prefrontal cortex (DLPFC) may mediate PD cognitive impairment and be a neuromodulation target for cognitive symptoms. We have previously shown caudate and DLPFC beta power contributes to working memory updating, and suppression of prefrontal cortex beta bursts during working memory encoding has been linked with improved performance. However, how PD affects beta bursting in relation to memory function remains unknown. METHODS: Fourteen PD patients undergoing awake DBS surgery with electrode trajectories traversing the caudate, DLPFC, or both participated in this study. Subjects completed a 2-back working memory task where they identified whether a presented word matched the word presented two trials prior. Bursts were defined as epochs where power exceeded a Z-score of two for at least three oscillatory cycles. We correlated change in caudate and DLPFC beta burst rates during working memory encoding with subjects’ composite memory scores, which were calculated from preoperative neuropsychological assessments. RESULTS: Caudate and DLPFC beta burst rates decreased significantly during working memory encoding for correct trials. In both structures, change in beta burst rate was significantly correlated with subjects’ composite memory scores, with greater decreases in beta bursting corresponding with better memory function. CONCLUSIONS: Beta bursts are suppressed in caudate and DLPFC during working memory encoding. Reduced beta burst suppression during encoding correlated with greater memory impairment in PD patients, indicating that altered caudate and DLPFC beta bursting dynamics may contribute to PD memory impairment.