Abstract

INTRODUCTION: Cognitive impairment (CI) is the most frequent nonmotor symptom in Parkinson’s Disease (PD) and is associated with deficits in executive functions such as working memory (Kehagia et al, 2010). Previous studies have demonstrated that caudate and DLPFC beta power underlie learning and working memory (Bick et al, 2019). Decreased dopamine in motor cortico-striato-thalamo-cortical (CSTC) circuits results in increased beta power and PD motor symptoms (Lapidus et al, 2014). Analogous changes in cognitive CSTC circuits, including the dorsolateral prefrontal cortex (DLPFC), may contribute to PD CI and be a target for neuromodulation. Better understanding of anatomic structures and neurophysiologic changes associated with working memory deficits is needed to develop potential neuromodulatory treatment strategies for PD CI. METHODS: Thirteen PD and ten ET patients who underwent deep brain stimulation in 2021 at Vanderbilt University Medical Center were consented and included in this analysis. Intraoperative local field potential recordings were obtained from the DLPFC during a 2-back verbal memory task with performance feedback (Owen et al, 2005). Signals were sampled at 1000Hz, Butterworth band pass filtered, de-meaned and averaged across patients. Average beta power differences 500-1000 msec following image onset were analyzed for correct and incorrect trials for PD and ET patients. RESULTS: PD patients exhibited significantly lower mean beta power compared to ET patients for correct trials (p = 0.0305, Wilcoxon rank-sum test). CONCLUSIONS: Neurophysiologic patterns underlying working memory encoding deficits in PD patients may reflect underlying dopaminergic dysfunction in cognitive CSTC circuits that result in CI. Structures within this circuit may be implicated in PD memory impairment and may serve as potential secondary targets for neuromodulation to improve working memory in patients with comorbid CI.

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