Corticostriatal Beta Power Changes Associated with Cognitive Function in Parkinson’s Disease

Abstract

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. Previous studies have demonstrated that caudate beta power is involved in learning and working memory. Decreased dopamine in motor cortico-striato-thalamo-cortical (CSTC) circuits results in increased beta power and PD motor symptoms. Analogous changes in cognitive CSTC circuits, including the caudate and dorsolateral prefrontal cortex (DLPFC), may contribute to PD CI. The objective of our study is to evaluate whether beta power changes in caudate and DLPFC contribute to cognitive impairment in PD patients. To investigate this, we used local field potential (LFP) recordings during deep brain stimulation surgery in 15 PD patients. LFP signals from DLPFC and caudate were performed at rest and during a verbal working memory task. We examined beta power changes during the working memory task and relationship of beta power to pre-operative neuropsychological testing results. Beta power decreased in both DLPFC and caudate during encoding of correct trials, whereas beta power increased in DLPFC and caudate during feedback for correct responses. Subjects with cognitive impairment showed smaller decreases in caudate and DLPFC beta power during encoding, greater increases in beta power during feedback, and lower average resting-state beta power. Additionally, reduced caudate beta power during encoding correlated with better memory scores on pre-operative neuropsychological testing, while greater DLPFC beta power during feedback correlated with worse scores in the attention domain. Our findings suggest that similar to the relationship between beta power in motor CSTC circuits and PD motor symptoms, beta power changes in parallel cognitive CSTC circuits may be correlated with cognitive symptoms in PD patients.